Table of Content

05 September 2026, Volume 46 Issue 9

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Original Articles

Hesperetin attenuates cartilage damage in mouse models of osteoarthritis

ZHANG Ziqiang, WANG Jie, GUAN Yunbo, SUN Xiaofei, LI Jian, WENG Tujun, WANG Zuqiang

2026, 46(9):  1167-1174.  doi:10.16352/j.issn.1001-6325.2026.09.1167

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Objective To evaluate the effect of hesperetin (HST) on cartilage damage in mouse models of destabilization in medial meniscus (DMM)-induced osteoarthritis, and to explore mechanisms. Methods 1)In vitro experiments: CCK-8 assay was used to evaluate the effect of hesperetin on bone marrow mesenchymal stem cells(BM-MSCs) viability. BM-MSCs chondrogenic induction model was established and chondrogenic differentiation was evaluated by type Ⅱ collagen(COL2)immunofluorescence staining microscopy; An IL-1β-induced chondrocyte inflammatory model was established, and real-time quantitative PCR was used to detect the expression of inflammation-related genes. 2) Animal experiments:A mouse DMM model of osteoarthritis was established, and hesperetin was administered by intra-articular injection. Gait analysis, histological staining, and Osteoarthritis Research Society International (OARSI) scoring were used to evaluate its effects. Results Within the concentration range of 0.4-10 μmol/L, hesperetin had no significant effect on BM-MSCs viability, whereas 50 μmol/L hesperetin reduced BM-MSCs viability(P＜0.05). Compared to the control group, hesperetin enhanced COL2 expression during BM-MSCs chondrogenic induction(P＜0.05). In IL-1β-stimulated chondrocytes, hesperetin downregulated the mRNA expression levels of IL-1β, IL-6, and TNF-α(P＜0.05). In the DMM mouse model, hesperetin improved gait abnormalities, alleviated cartilage damage and reduced OARSI scores(P＜0.05). Conclusions In osteoarthritis of DMM mouse models, hesperetin alleviated cartilage damage. Its effects may be associated with the promotion of BM-MSCs chondrogenic differentiation and inhibition of inflammation-related gene expression in chondrocytes under inflammatory stimulation.

LINC00339 promotes the migration and invasion of thyroid cancer cell lines by regulating the miR-15b-5p/E2F3 axis

ZHANG Youliang, REN Guangyu, WU Jia, ZHU Haohao

2026, 46(9):  1175-1182.  doi:10.16352/j.issn.1001-6325.2026.09.1175

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Objective To investigate the role of long non-coding RNA LINC00339 in the migration and invasion of thyroid cancer (TC) cells and its molecular mechanism. Methods Thyroid cancer cell line KTC-1 was divided into sh-NC group, sh-LINC00339 group, NC mimic group, miR-15b-5p mimic group, NC inhibitor group, miR-15b-5p inhibitor group, sh-LINC00339+NC inhibitor group, sh-LINC00339+miR-15b-5p inhibitor group, miR-15b-5p mimic+pcDNA-NC group, miR-15b-5p mimic+pcDNA-E2F3 group, sh-LINC00339+pcDNA-NC group and sh-LINC00339+ pcDNA-E2F3 group. Three holes were set in each group. The expression levels of LINC00339, miR-15b-5p and E2F3 mRNA were detected by RT-qPCR. Wound healing assay and Transwell assay were used to evaluate the ability of cell migration and invasion. Tumor sphere formation assay was used to detect the characteristics of stem cells. Western blot was used to detect the protein expression of stemness-related markers. Results Compared with normal thyroid cells, the expression of LINC00339 and E2F3 in TC cell lines was up-regulated, and the expression of miR-15b-5p was down-regulated (P＜0.05). Interfering with LINC00339 can reduce the expression of E2F3, inhibit cell migration, invasion and stem cell characteristics, and up-regulate miR-15b-5p. Inhibition of miR-15b-5p partially reversed these effects (P＜0.05). Over-expression of miR-15b-5p could inhibit E2F3 expression and cell migration, invasion and stem cell characteristics, while over-expression of E2F3 could restore these effects (P＜0.05). Conclusions LINC00339 is highly expressed in TC cell lines, which can relieve the inhibitory effect of miR-15b-5p on E2F3 by targeting down-regulation of miR-15b-5p expression, thereby inducing the stem cell characteristics of TC cell lines and promoting cell migration and invasion.

Rock salt aerosol regulates Th17/Treg immune balance and alleviates airway inflammation in patients with pneumoconiosis combined with COPD

HOU Tingting, BAO Zhen, DOU Hong

2026, 46(9):  1183-1188.  doi:10.16352/j.issn.1001-6325.2026.09.1183

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Objective To investigate the effects of rock salt aerosol (RSA) on airway inflammation in patients with pneumoconiosis combined with chronic obstructive pulmonary disease (COPD) through modulating Th17/Treg immune balance. Methods A prospective randomized controlled test enrolled 86 patients with pneumoconiosis and COPD, who were randomly assigned to a RSA group or control group. Both groups received standardized basic treatment then the RSA group inhaled RSA and the control group inhaled saline aerosol for 24 weeks. Pulmonary function tests, blood gas analysis, inflammatory markers, Th17/Treg immune balance indicators, and clinical symptoms were recorded to evaluate treatment efficacy. Results A total of 41 patients in the RSA group and 40 in the control group completed the study. The RSA group showed significantly better improvements in pulmonary function parameters, blood gas status, and inflammatory factors (IL-6, IL-8) as compared to the control group (P＜0.05). The RSA group also demonstrated a reduced Th17 cell proportion, increased Treg cell proportion and a more significant decrease in the Th17/Treg ratio (P＜0.001). Clinical symptom scores were lower, with a total effective rate of 90.24% (compared to 52.50% in the control group, P＜0.001). Correlation analysis revealed that the Th17/Treg ratio in the RSA group was positively correlated with inflammatory factors and negatively correlated with pulmonary function. Conclusions RSA effectively improves pulmonary function and clinical symptoms of pneumoconiosis patients complicated with COPD. Its mechanism may involve regulation of Th17/Treg balance and inhibition of airway inflammation.

Crocin alleviates retinal ischemia-reperfusion injury in rat models by inhibition of ferroptosis

WANG Shuangmei, XUE Fang, FENG Yan, ZHU Jinyifu, YANG Xinguang, YU Jingni

2026, 46(9):  1189-1199.  doi:10.16352/j.issn.1001-6325.2026.09.1189

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Objective To find potential effect of crocin (Cro) to alleviate retinal ischemia-reperfusion injury (RI/RI) in rat′s model. Methods Rats were divided into 6 groups (n=12): sham operation group (sham), RI/RI group (rats with RI/RI model established by intraocular perfusion), 25Cro group, 50Cro group (intraperitoneal injection of 25 and 50 mg/kg Cro, respectively), 50Cro+OSS (OSS_128167) group (intraperitoneal injection of 50 mg/kg Cro and 20 mg/kg Sirt6 inhibitor OSS), and 50Cro+Erastin group (intraperitoneal injection of 50 mg/kg Cro and 15 mg/kg ferroptosis inducer Erastin). The administration time was 30 min before RI/RI modeling. Rats were sacrificed 24 h after RI/RI treatment, retinal injury and cell apoptosis were evaluated by hematoxylin-eosin (HE) staining microscopy and terminal deoxynucleotidyl transferase mediated dUTP nick end-labeling (TUNEL) staining. The level of reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), reduced glutathione (GSH) and Fe²⁺ in the retina was detected. The mRNA level of Sirt6, glutathione peroxides 4(Gpx4), solute carrier family 7 member 11(Slc7a11), ferritin heavy chain 1(Fth1), ferroportin 1(Fpn1), transferrin receptor (Tfrc), interleukin-6(Il-6), tumor necrosis factor-α(Tnf-α) and cyclooxygenase-2 (Cox-2) in the retina was detected by RT-qPCR. The protein level of Sirt6, GPX4, B-cell lymphoma 2 (Bcl-2), Bcl-2 associated X protein (Bax) and cleaved caspase-3 in the retina was detected by Western blot. The positive expression of Sirt6 and GPX4 in the retina was detected by immunohistochemical staining. Results Compared with sham group, the retina of rats in RI/RI group showed significant damage. The proportion of TUNEL⁺ in the retina, the level of ROS, MDA and Fe²⁺, mRNA of IL-6, TNF-α, COX-2 and TFRC, and the protein level of Bax and cleaved caspase-3 were all increased(P＜0.05). The level of GSH and SOD activity, the mRNA level of Fth1, Fpn1, Gpx4, Slc7a11 and Sirt6, and the protein level of Bcl-2, GPX4 and Sirt6 were all decreased (P＜0.05). Compared with RI/RI group, the retinal damage in 25Cro group and 50Cro group was significantly alleviated, and the other indicators were significantly relieved (P＜0.05). Compared with 50Cro group, the retinal injury of rats in 50Cro+OSS group and 50Cro+Erastin group were exacerbated. The proportion of retinal TUNEL⁺, the level of ROS, MDA and Fe²⁺, the mRNA levels of Il-6, Tnf-α, Cox-2 and Tfrc, and the protein levels of Bax and cleaved caspase-3 all increased (P＜0.05). The levels of GSH and SOD activity, the mRNA levels of Fth1, Fpn1, Gpx4, Slc7a11 and Sirt6, and the protein level of Bcl-2, GPX4 and Sirt6 was all decreased (P＜0.05). Conclusions Crocin alleviates RI/RI in rats by inhibition of Sirt6-mediated ferroptosis.

Pristimerin sensitizes human esophageal squamous cell carcinoma cell strain ECA109/DDP to cisplatin

LIU Guiju, YUAN Wei, LYU Dinglin, HAN Qianqian, MEI Jiazhuan, ZHANG Haozhe

2026, 46(9):  1200-1206.  doi:10.16352/j.issn.1001-6325.2026.09.1200

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Objective To investigate the mechanism by which pristimerin enhances cis-diamine dichloroplatinum/cisplatin(DDP) sensitivity of esophageal squamous cell carcinoma cell line ECA109. Methods ECA109 cells were treated with 20 μg/mL DDP, with drug concentrations incrementally increased (40, 80, 100 μg/mL) every 2-3 passages. After 3-6 months, stable DDP-resistant ECA109/DDP cells were obtained which proliferated in high DDP concentration environment (80 μg/mL). The ECA109/DDP cells were divided into the following groups: control, DDP (80 μg/mL), pristimerin (1 μmol/L), pristimerin (1 μmol/L)+DDP (80 μg/mL), and pristimerin (1 μmol/L)+DDP (80 μg/mL)+TGF-β activator (SRI-011381) (10 μmol/L). Cell proliferation was assessed by CCK-8 assay and colony formation test; Apoptosis was examined by flow cytometry; Migration and invasion were evaluated via scratch wound healing and Transwell assays, respectively. The protein expressions of multidrug resistance-associated protein 1 (MRP1), P-glycoprotein (P-gp), TGF-β1, Smad4, and CD44 were measured by Western blot. Results Compared with control group, there was no difference in various indicators in the DDP group(P＜0.05). While pristimerin group exhibited a decrease of A₄₅₀ values, colony formation rate, scratch healing rate, number of invasive cells. The protein level of MRP1, P-gp, TGF-β1, Smad4, and CD44 also decreased, along with increased apoptosis (P＜0.05). Compared with the DDP and pristimerin groups, the pristimerin+DDP group showed further reduction in A₄₅₀ values, colony formation rate, scratch healing rate, number of invasive cells, and protein level of MRP1, P-gp, TGF-β1, Smad4, and CD44, as well as increased apoptosis (P＜0.05). Compared with pristimerin+DDP group, pristimerin+DDP+SRI-011381 group showed an opposite trend in all the above indicators (P＜0.05). Conclusions Pristimerin enhances DDP sensitivity in ECA109/DDP cells by inhibition of TGF-β/Smad pathway.

Parthenolide alleviates sepsis-induced acute lung injury in rat models by regulating the ferroptosis pathway

ZHANG Lulu, TIAN Hui

2026, 46(9):  1207-1212.  doi:10.16352/j.issn.1001-6325.2026.09.1207

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Objective To explore the effect of parthenolide (PTL) on sepsis-induced acute lung injury (ALI) through nuclear factor erythroid 2-related factor 2-glutathione peroxidase 4 (Nrf2-GPX4) ferroptosis pathway. Methods The cecal ligation and puncture (CLP) method was used to construct an ALI rat model. Rats were randomly divided into control group, ALI group, ALI+PTL group, ALI+Nrf2 agonist (SFN) group, and ALI+PTL+Nrf2 inhibitor (ML385) group. Blood gas indicators and pulmonary edema were evaluated by Blood gas analyzer and lung wet/dry weight ratio. HE staining and Perls staining microscopy were used to identify the pathological characteristics. ELISA and immunofluorescence were performed to measure oxidative stress and iron metabolism indicators. Western blot was performed to detect the Nrf2-GPX4 pathway related proteins. Results ALI group, ALI+PTL group and ALI+SFN group all showed up-regulation of partial arterial pressure of oxygen(PaO₂), superoxide dismutase(SOD) activity, glutathione peroxidase(GSH-Px) activity, glutathione peroxidase 4(GPX4) positive cell rate, p-Nrf2/Nrf2 ratio, and GPX4 protein, but down-regulation of partial arterial pressure of carbon dioxide(PaCO₂), lung wet/dry weight ratio, lung tissue pathological injury score, iron deposition area percentage, 4-hydroxynonenal(4-HNE) content, 8-hydroxy-2-deoxyguanosine(8-OHdG) content, acyl-CoA synthetase long-chain family member 4(ACSL4) positive cell rate, ferritin positive cell rate and heme oxygenase-1(HO-1) protein(P＜0.05). In ALI+PTL group and ALI+PTL+ML385 group indicators mentioned above were all significantly reversed(P＜0.05). Conclusions PTL alleviates sepsis-induced ALI by a mechanism of activation of Nrf2-GPX4 pathway.

Bufei-Huoxue formula (BFHX) alleviates pulmonary inflammatory injury in rat models with COPD by regulating the SphK1/S1P signaling pathway

LI Xiaoying, LI Xiaodan, LI Yuqian, LI Shanshan, LI Tiange

2026, 46(9):  1213-1220.  doi:10.16352/j.issn.1001-6325.2026.09.1213

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Objective To investigate the effect of Bufei-Huoxue formula (BFHX) on inflammatory injury in the lung tissue of rat model with chronic obstructive pulmonary disease (COPD). Methods Rat model of COPD was established by endotracheal infusion of lipopolysaccharide (LPS) combined with smoking stimulation. Rats were randomly assigned into model group, positive drug ambroxol (positive) group, low- and high-dose BFHX (BFHX-L, BFHX-H) groups, and high-dose BFHX+SphK1/S1P pathway activator (BFHX-H+PMA) group. The control group consisted of 8 healthy rats. The lung function of rats was examined, and the level of inflammatory cytokines in bronchoalveolar lavage fluid (BALF) was measured by ELISA. The pathological changes of lung tissue were detected by HE staining, bronchial mucus secretion was measured by AB-PAS staining and pulmonary fibrosis was measured by Masson staining. The expression of Muc5ac protein in lung tissue was measured by immuno-histochemistry and the expression of SphK1,S1P,α-SMA,ColⅠ and TGF-β proteins was detected by Western blot. Results Compared with the control group, rats in the model groups exhibited decreased lung function and aggravated pulmonary fibrosis accompanied by elevated level of TNF-α,IL-6,and IL-8 in BALF, increased bronchial mucus secretion and collagen volume fraction,Muc5ac positive expression and protein expression level of SphK1,S1P,α-SMA,ColⅠ,and TGF-β in lung tissue, as well as a reduced level of IL-10(P＜0.05). Compared with the model groups, the BFHX-treated group and positive group showed improved pulmonary function and alleviated histo-pathological damage of lung tissue. Additionally The level of TNF-α,IL-6,and IL-8 in BALF, bronchial mucus secretion in lung tissue, collagen volume fraction, positive expression of Muc5ac,as well as the protein expression of SphK1,S1P,α-SMA, ColⅠand TGF-β were all significantly decreased, while the level of IL-10 was markedly increased(P＜0.05). Compared with BFHX-H group, the BFHX-H+PMA group exhibited aggravated histo-pathological damage and impaired pulmonary function in lung tissue. Furthermore, the levels of TNF-α,IL-6,and IL-8 in BALF,the amount of bronchial mucus secretion in lung tissue collagen volume fraction, the positive expression of Muc5ac,as well as the protein expression levels of SphK1,S1P,α-SMA,ColⅠ,and TGF-β were also significantly increased, but the level of IL-10 was markedly decreased(P＜0.05). Conclusions BFHX alleviates airway mucus hyper-secretion and pulmonary fibrosis in COPD rat models and improve lung tissue inflammatory injury and lung function. Its mechanism of action potentially related to the reduction of SphK1/S1P pathway activity.

Remimazolam pretreatment alleviates liver injury in rat models with liver ischemia-reperfusion

XUE Xiaohong, HE Shan, SUN Lingshuang, SONG Keke, HUANG Jian, ZHOU Rongsheng

2026, 46(9):  1221-1226.  doi:10.16352/j.issn.1001-6325.2026.09.1221

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Objective To investigate the effects of remazolam (REM) pretreatment on systemic oxidative stress, inflammation and apoptosis of liver cells in hepatic ischemia-reperfusion injury (HI/RI) rats. Methods Thirty SPF-grade male SD rats with body weight of 220-280 g, were randomly divided into 3 groups (n=10): sham operation group (sham group, only laparotomy), model group (HI/R group, a model was established with 70% liver ischemia for 60 minutes and then reperfusion for 6 hours), and intervention group (REM group, REM 10 mg/kg was injected via the tail vein 10 minutes before liver ischemia). Six hours after reperfusion, the rats were euthanized and vena cava blood and specimens of the left lobe of the liver were collected. Serum AST and ALT level were detected using an automatic biochemical analyzer. Serum level of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 was measured by ELISA. Hepatic histo-pathological changes were observed using HE staining microscopy. The content of MDA was detected by thiobarbituric acid (TBA), and the activity of SOD was checked by xanthine oxidase (XOD). The expression of apoptosis-related proteins Bax and Bcl-2 was detected by Western blot. The apoptosis index (AI) of liver tissue cells was detected by TUNEL. Results After ischemia-reperfusion treatment, the expression of serum liver enzymes(AST,ALT) and pro-inflammatory mediators(TNF-α, IL-1β, IL-6) in the HI/R group were significantly higher than those in the sham group(P＜0.01). The expression of lipid peroxidation product MDA and pro-apoptotic protein Bax in liver tissue was significantly increased(P＜0.01). The activity of endogenous antioxidant enzyme SOD and the expression of anti-apoptotic protein Bcl-2 and AI of liver cells were significantly decreased(P＜0.01). After pretreatment with remimazolam, the expression levels of AST, ALT, TNF-α, IL-1β and IL-6 in the serum of the REM group were significantly lower than those in the HI/R group(P＜0.01). The expression of MDA and Bax protein in liver tissue was significantly decreased(P＜0.01). While the activity of SOD and the expression of Bcl-2 protein were significantly increased(P＜0.01). The AI of liver cells was significantly decreased(P＜0.01). Conclusions REM pretreatment can alleviate HI/R-induced hepatic dysfunction via multi-targeted mechanisms: inhibition of systemic oxidative stress, reduction of inflammation and alleviation of hepatocyte apoptosis.

SLCO2A1 mutation-mediated vascular endothelial cell dysfunction contributes to chronic enteropathy(CEAS) development and progression

ZHANG Yiyao, YUN Longxi, HUANG Jingyi, LI Xiaoyu, YUAN Jingyi, LI Yue, LIU Changzheng

2026, 46(9):  1227-1236.  doi:10.16352/j.issn.1001-6325.2026.09.1227

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Objective To investigate the pathogenic mechanism of chronic enteropathy associated with SLCO2A1 with SLCO2A1 gene(CEAS), a hereditary disease caused by SLCO2A1 mutations, and to provide theoretical insight into potential therapeutic strategies. Methods Molecular docking was performed to model the binding structure between prostaglandin E2(PGE₂) and SLCO2A1. PGE₂ levels in urine and peripheral blood were measured by ELISA. CD31 and IGFBP7 expression in intestinal tissues was assessed by immunohistochemistry. Public databases were used to confirm the high expression of SLCO2A1 in endothelial cells. Human umbilical vein endothelial cells(HUVECs) were used as an in vitro model, and SLCO2A1 was knocked down by siRNA. Fluorescent PGE₂ uptake assays, tube formation assays, and transcriptomic sequencing were performed to evaluate functional changes. Exogenous PGE₂ and indomethacin were further used to mimic pathological intra- and extracellular PGE₂ accumulation, followed by assessment of angiogenesis and transcriptomic alterations. Results CEAS patients showed an increased urinary PGE₂ levels(P＜0.01) but a decreased peripheral blood PGE₂ level(P＜0.001). Intestinal tissues exhibited reduced CD31 expression(P＜0.001) and increased IGFBP7 expression(P＜0.05). SLCO2A1 knockdown in HUVECs significantly impaired PGE₂ uptake and reduced angiogenic capacity(P＜0.05). Transcriptomic analysis revealed enrichment of differentially expressed genes in pathways related to cell communication, JAK-STAT signaling, and calcium signaling. After exogenous PGE₂ treatment, angiogenesis remained lower in SLCO2A1-knockdown cells than in controls(P＜0.000 1), accompanied by sustained activation of the JAK/STAT pathway(P＜0.000 1). Indomethacin inhibited angiogenesis only in wild-type cells(P＜0.000 1) and had no significant effect on SLCO2A1-knockdown cells. Conclusions SLCO2A1 deficiency disrupts PGE₂ transport and leads to an abnormal extracellular PGE₂ accumulation. This process may inhibit endothelial angiogenesis through sustained activation of JAK/STAT-mediated inflammatory signaling, thereby contributing to CEAS progression.

Midazolam alleviates brain injury in rat models caused by cerebral ischemia-reperfusion

ZUO Yong, SI Yuting, WANG Yang, ZHAO Xiaoliang

2026, 46(9):  1237-1242.  doi:10.16352/j.issn.1001-6325.2026.09.1237

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Objective To investigate the effect of midazolam (MDZ) on brain injury in rats with cerebral ischemia-reperfusion injury(CI/RI). Methods Rats with CI/RI were divided into five groups: CI/RI group, MDZ-L group (intravenous injection of 0.05 mg/kg MDZ), MDZ-M group (0.15 mg/kg MDZ) and MDZ-H group (0.30 mg/kg MDZ). Additionally, there was an MDZ-H + verteporfin(inhibitor of Hippo/YAP signaling pathway) group (intraperitoneal injection of 10 mg/kg verteporfin). The control group received an equivalent volume of saline.Outcomes were evaluated by neurological deficits,infarct volume, histopathological changes in brain tissue, neuronal apoptosis, inflammatory cytokines and related protein expression. Results The CI/RI group showed loosening of neuronal arrangement, enlarged cell bodies, and nuclear shift as compared to the control group. The brain tissue damage was less severe in the MDZ-L, MDZ-M, and MDZ-H groups as compared to the CI/RI group. The MDZ-H + verteporfin group exhibited more severe brain tissue damage than the MDZ-H group. The CI/RI group showed increased neurological deficit scores, infarct volume, level of TNF-α and IL-1β in brain tissue, and neuronal apoptosis rate as compared to the control group, while the expression of YAP and TAZ proteins in brain tissue was decreased (P＜0.05). The MDZ-L, MDZ-M, and MDZ-H groups showed a decrease in neurological deficits, infarct size, inflammatory cytokines and apoptosis rate, along with increased YAP and TAZ protein expression compared to the CI/RI group (P＜0.05). The MDZ-H + verteporfin group showed a reversal picture of these indicators (P＜0.05). Conclusions MDZ can partially activate the Hippo/YAP signaling pathway and reduce brain tissue damage.

Midazolam alleviates cartilage injury and pain in rat models with monosodium iodoacetate-induced osteoarthritis

YANG Chunhui, XIAO Ting, LIU Hua, YANG Kunqing

2026, 46(9):  1243-1248.  doi:10.16352/j.issn.1001-6325.2026.09.1243

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Objective To investigate the effects and mechanism of midazolam (MDZ) on cartilage damage and pain in a rat model of osteoarthritis (OA) induced by monosodium iodoacetate (MIA). Methods OA rat models were divided into following groups: OA, low, medium, and high-dose MDZ (30, 60, 90 mg/kg), high-dose MDZ+compound C (0.2 mg/kg via tail vein) and control group with in each. Behavioral performance was assessed using the modified Lequesne MG scale. Joint pain was measured, and level of MMP-1, COX-2, and IL-1 in joint fluid was measured by ELISA method. Cartilage damage was examined by histology with Van Gieson and toluidine blue staining microscopy. AMPK/SIRT1/NF-κB pathway related proteins were detected by Western blot. Results OA rats showed superficial cartilage staining loss, thinning of cartilage layers, and incomplete tide lines. MDZ groups showed reduced cartilage damage, but more significant damage in the MDZ-H+compound C group. OA rats had higher Lequesne and Mankin scores, MMP-1, COX-2, IL-1 levels, and p-NF-κB p65 expression, while p-AMPK/AMPK and SIRT1 were all decreased (P＜0.05). MDZ treatments decreased these scores and markers dose-dependently, with some reversal trends seen in the MDZ-H+compound C group. Conclusions MDZ can partially activate the AMPK/SIRT1/NF-κB signaling pathway, thereby alleviating cartilage damage and pain in rats with OA.

Clinical Sciences

Nenroimaging analysis of 30 cases of patients with acute intermitent porphyria

LIU Yanting, CAO Jian, HAN Fei, ZHU Huadong, LI Yi, LIU Anlei, YANG Jing

2026, 46(9):  1249-1255.  doi:10.16352/j.issn.1001-6325.2026.09.1249

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Objective To elucidate the neuroimaging changes and clinical relevances of acute intermittent porphyria (AIP) patients with neurological symptoms by analyzing the clinical features and neuroimaging findings. Methods 30 cases of AIP were described, focusing on their neurological clinical features and neuroimaging findings. Urinary porphobilinogen (PBG) was quantitatively screened using the Watson-Schwartz method. During porphyric attacks, brain computed tomography (CT) and/or magnetic resonance imaging (MRI) as well as electroencephalography blood sodium levels and cerebrospinal fluid (CSF) examinations were performed in some patients. Genetic screening for AIP was also performed in families who consented to genetic testing. Molecular genetic analysis of the hydroxy-methylbilane synthase (HMBS) was conducted by direct sequencing of peripheral blood samples. Results 30 AIP patients were all females, and the clinical manifestations were various, including consciousness disturbance (n=18), convulsion (n=17), muscle weakness (n=14), abdominal pain (n=29) and tachycardia (n=21). Based on the neuroimaging, two porphyric encephalopathy (cortical laminar necrosis), four posterior reversible encephalopathy syndrome (PRES), four osmotic demyelination syndromes (ODS) and one reversible splenial lesion syndrome (RESLES) were identified. The blood sodium levels of abnormal MRI/CT group were significantly lower than that of normal MRI/CT group[(110.8±6.5)mmol/L vs. (118.4±7.8)mmol/L, P＜0.01].25 cases of pathogenic mutations were detected. Conclusions Cortical laminar necrosis, PRES, ODS, and RESLES represent patterns of central nervous system(CNS) involvement in AIP. Hyponatremia may be an important mechanism in porphyric encephalopathy.

Interference factors affecting the accuracy of flash glucose monitoring after pancreatic surgery

LAN Ling, ZHANG Le, ZHANG Yuelun, SHEN Le, HUANG Yuguang

2026, 46(9):  1256-1261.  doi:10.16352/j.issn.1001-6325.2026.09.1256

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Objective To explore the factors affecting the numerical accuracy of flash glucose monitoring (FGM) system in patients after pancreatic surgery. Methods A retrospective analysis was conducted on 279 adult patients who underwent elective pancreatic surgery at Peking Union Medical College Hospital from March 2024 to March 2025. Finally, 255 cases were included. All patients wore FGM sensors on the dorsum of the left upper arm one day before surgery, and received point-of-care (POC) capillary blood glucose measurements at least twice postoperatively. The reference blood glucose values were contemporaneous POC blood glucose readings. Paired matching was performed by taking the time points of POC blood glucose detection as benchmarks, and retrieving the closest FGM readings in the Gplus system for pairing. The mean absolute difference of paired blood glucose values was calculated for each subject. LASSO regression was used for variable selection, and Bootstrap resampling was applied to evaluate the occurrence frequency of screened variables. Multiple linear regression analysis was adopted to investigate the correlation between relevant variables and the mean difference of paired blood glucose values. Results The median mean difference between FGM readings and POC blood glucose values was 1.2 mmol/L. Multiple linear regression analysis revealed that maximum postoperative blood glucose (β=0.082, 95% CI: 0.055-0.108, P＜0.001), intraoperative crystalloid infusion (per 1L increment, β=0.124, 95% CI: 0.054-0.194, P＜0.001), jaundice (β=0.215, 95% CI: 0.019-0.412, P＜0.05) and age (per decade increase, β=0.091, 95% CI: 0.031-0.150, P＜0.05) were linearly correlated with the natural logarithm of the mean paired blood glucose difference(R_adj²=0.245). Conclusions Age, jaundice, intraoperative crystalloid infusion volume and maximum postoperative blood glucose are independent influencing factors for postoperative FGM accuracy. Elevations of these indicators are linearly correlated with greater FGM deviation.

Comparison of diagnostic performance between ultrasound-guided core needle biopsy and fine-needle aspiration in subclavian lymph node biopsy

ZHOU Jianyu, SUN Yuanyuan, SANG Lin, ZHOU Huihui, GONG Xue

2026, 46(9):  1262-1266.  doi:10.16352/j.issn.1001-6325.2026.09.1262

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Objective To compare the diagnostic performance and safety profiles between ultrasound-guided core needle biopsy (CNB) and fine-needle aspiration (FNA) for infraclavicular lymph node biopsy, and establish a stratified decision-making framework based on anatomical characteristics and patient risk factors. Methods This retrospective study analyzed 561 consecutive cases of infraclavicular lymph node biopsies. Patients were stratified into CNB group (n=282, lymph node transverse diameter ≥1.0 cm) and FNA group (n=279, transverse diameter ＜1.0 cm or with advanced age/coagulopathy). The diagnostic efficacy and complications between two groups were collected and compared. Patients were divided into 2 groups based on the occurrence of complications, and multivariate Logistic regression analysis was performed to identify risk factors for complications. Results The diagnostic accuracy (98.20% vs. 93.50%), sensitivity (96.90% vs. 90.30%) and negative predictive value(96.00% vs.83.80%) of CNB group were significantly higher than those of the FNA group (P＜0.01). The incidence of complications such as puncture site bleeding and mild pain in the CNB group was 28 cases (9.93%), significantly higher than the 8 cases (2.87%) in the FNA group (χ²=11.646, P＜0.01). Age, puncture method and longitudinal diameter of the lymph node were independent influencing factors for complications after subclavian lymph node biopsy (P＜0.05). Conclusions For subclavian lymph node biopsy, CNB demonstrates superior diagnostic performance but carries a higher risk, while FNA is safer but may lead to missed diagnoses. Clinical decisions should prioritize precision individualized puncture based on lymph node size and patient-specific factors, such as age, coagulation abnormalities.

Analysis of clinical characteristics, diagnosis and management in 28 cases of mesenteric panniculitis

LU Junyang, LIU Anlei, ZHOU Kang, WANG Qiang, XIAO Yinbo, DAI Jiayuan, SHEN Min

2026, 46(9):  1267-1271.  doi:10.16352/j.issn.1001-6325.2026.09.1267

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Objective To summarize the clinical characteristics of mesenteric panniculitis (MP) in order to further enhance the understanding of this disease. Methods Retrospective analysis was conducted on hospitalized patients with a definite diagnosis of mesenteric panniculitis at Peking Union Medical College Hospital from January 2015 to January 2026. The clinical characteristics and treatment status of the patients were analyzed. Results A total of 28 patients were included. There were 13 males (46.4%) and 15 females (53.6%), with a mean age of (58.14±10.87) years. Abdominal pain was the most common chief complaint (96.4%), followed by abdominal distension(14.3%), fever (10.7%), nausea and vomiting (3.6%), and diarrhea (3.6%). Eighteen patients (64.3%)received corticosteroid therapy, among whom 7 received corticosteroids combined with immunosuppressive therapy,4 received corticosteroids combined with biologic agents, and 1 received corticosteroids combined with tamoxifen.Four patients underwent surgery; two of them had mesenteric lesion resection but experienced recurrence three months postoperatively. During follow-up, 18 patients remained stable, one patient treated with corticosteroid immunotherapy showed no response, one relapsed after drug discontinuation, and two were lost to follow-up. Conclusions MP is a chronic inflammatory disease. Patients typically present with abdominal pain as the predominant symptom, and the prognosis is generally favorable after accurate diagnosis and appropriate treatment. This study aims to provide a basis for improving clinicians′ understanding of mesenteric panniculitis, in order to avoid misdiagnosis or missed diagnosis.

Case Reports

One case report of a 45 cm retroperitoneal dedifferentiated liposarcoma

WANG Jun, HUA Yiwei, ZHAO Yi, LIU Guanghua, DONG Jie

2026, 46(9):  1272-1276.  doi:10.16352/j.issn.1001-6325.2026.09.1272

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Objective To investigate the clinical characteristics, diagnostic process, surgical treatment and peri-operative management of retroperitoneal dedifferentiated liposarcoma (DDLPS) and to improve awareness of this type of rare giant tumor while providing a reference for future clinical diagnosis and treatment. Methods A case of a 57-year-old male patient admitted to the Department of Urology, Peking Union Medical College Hospital in September 2025. The patient′s electronic medical records were retrospectively reviewed, including outpatient and inpatient records, laboratory and radiology results, and treatments during hospitalization. Results Physical examination revealed a giant palpable mass in the left abdomen. Radiology imaging showed significant displacements of the spleen, pancreas, left kidney, and left adrenal gland by the tumor and a compressed left ureter, resulting in upper urinary tract hydronephrosis. After en bloc resection, the tumor measured up to 45 cm in maximum diameter and weighed approximately 12.5 kg. Pathological fluorescence in situ hybridization (FISH) demonstrated amplification of murine double minute 2 (MDM2), supporting the diagnosis of DDLPS. The patient recovered uneventfully after surgery, was discharged on postoperative day 11, and remained in generally good condition at the 1-month follow-up. Conclusions The case demonstrated complex imaging features, since DDLPS with polymorphic calcification is relatively rare. For retroperitoneal masses of this size, diagnosis should be established based on a combination of imaging findings, pathological examination, and MDM2 amplification testing. Adequate preoperative assessment and complete surgical resection are also essential for relieving compression-related symptoms and improving prognosis.

Mini Reviews

Progress in ubiquitin-specific protease 1 of tumors

LIU Lindi, LIU Xuyan, LYU Qingjie

2026, 46(9):  1277-1281.  doi:10.16352/j.issn.1001-6325.2026.09.1277

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Ubiquitin-specific protease 1 (USP1) is an important member of the deubiquitinase family. It participates in biological processes such as DNA damage repair by regulating the stability of key proteins. USP1 is abnormally expressed in various tumors, and its expression level is closely related to tumor initiation, progression, metastasis and prognosis. Abnormal USP1 expression in multiple cancer cell types regulates cancer cell development through affecting biological processes including DNA damage repair, epithelial-mesenchymal transition, autophagy, cell cycle and mitochondrial fission. In-depth analysis of USP1 function and mechanism involved in various cancer cells provides a theoretical basis for diagnosis, prevention and treatment, as well as the development of USP1-targeted drugs.

Research advances in endogenous exosomes regulating ferroptosis pathways in related diseases

GAO Xuechu, HAN Shaofang, LIU Lingying

2026, 46(9):  1282-1286.  doi:10.16352/j.issn.1001-6325.2026.09.1282

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Ferroptosis is a novel form of iron-dependent programmed cell death, characterized by lipid peroxidation and iron accumulation which lead to an imbalance in host′s antioxidant defense system. Endogenous exosomes refer to extracellular vesicles secreted by cells within the organism. By transferring their cargo (such as lipids, proteins, and nucleic acids from the parent cells), which regulate ferroptosis through various signaling pathways, including Xc^-/GSH/GPX4 pathway, NAD(P)H/FSP1/CoQ10 pathway, iron metabolism pathway, and lipid metabolism pathway, thereby promotes disease progression in conditions such as hepato-cellular carcinoma, glioblastoma, heart disease, small cell lung cancer, esophageal cancer, ovarian cancer, gastric cancer, cervical cancer,sepsis-associated encephalopathy, hepatitis B and acute respiratory distress syndrome. Research focusing on the specific molecular mechanisms by which endogenous exosomes regulate ferroptosis in different diseases may explore new therapeutic targets and put insights into the diagnosis and treatment of related diseases.

Research progress on the mechanism of action of sterol regulatory element-binding protein(SREBP) in metabolic inflammatory syndrome

ZHANG Yi, YANG Lijuan, WANG Pingle

2026, 46(9):  1287-1292.  doi:10.16352/j.issn.1001-6325.2026.09.1287

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Sterol regulatory element-binding proteins(SREBPs), key transcription factors in cellular lipid metabolism regulation, play a significant role in the development of metabolic inflammatory response syndrome(MIS). Under prolonged high-fat intake, aberrant expression levels of SREBPs contribute to the pathogenesis of MIS by modulating multiple signaling pathways, including uric acid metabolism, vascular endothelial cell(VEC) proliferation, immune cell activity, and NF-κB/NLRP3 signaling pathway. Furthermore, excessive activation of SREBPs leads to chronic inflammation and impairs the body's ability to regulate inflammation.

Role of disulfidptosis in osteoarthritis

LI Na, MA Likai, ZHANG Junlei, DING Ning, MA Li

2026, 46(9):  1293-1297.  doi:10.16352/j.issn.1001-6325.2026.09.1293

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Disulfidptosis is a newly fond form of program cell death. Its core mechanism is characterized by cystine transporter solute carrier family 7 member 11(SLC7A11) expression, glucose deprivation leading to nicotinamide adenine dinucleotide phosphate(NADPH) depletion, impaired reduction and subsequent abnormal accumulation of cystine which triggers disulfide stress. This stress then attacks actin, and the damage is amplified through the Rac1-WRC pathway causing irreversible cytoskeleton collapse. Dysregulated expression of disulfidptosis-related genes influences the progression of osteoarthritis through multiple mechanisms, including inducing chondrocyte death, modulating chondrocyte-immune cell crosstalk to promote the inflammatory microenvironment of osteoarthritis, and determining the molecular heterogeneity of osteoarthritis. Targeting key molecules like SLC3A2 alleviate pathological changes in experimental models, indicating the therapeutic potential of targeting disulfidptosis.

Medical Education

Artificial intelligence supports digital transformation of “Molecular Biology Experiments of the Gene” course

FU Jun, ZHANG Zhuqin, HAN Wei, ZHANG Ran, LIANG Junbo, GU Jingli, XU Yuanyuan, PENG Xiaozhong

2026, 46(9):  1298-1301.  doi:10.16352/j.issn.1001-6325.2026.09.1298

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Objective Utilizing artificial intelligence(AI) to support education, and to explore the application in course of “Molecular Biology Experiment of the Gene” through a blended teaching approach which combined online and off-line instruction. Methods Totally 100 students in the academic year 2025—2026 at Peking Union Medical College were selected as the research subjects. Students were required to preview and review course-related theoretical knowledge, experimental procedures and precautions before and after class online. This study investigated the effectiveness of course digital transformation through various aspects such as students′ test scores, classroom performance, and feedback from post-class student surveys. Results The digital transformation of the course helped students in understanding experimental theories, familiarizing themselves with experimental operations, and paying attention to experimental precautions, which has been well received by students. There has been a significant improvement in students′ scores on in-class quizzes, and an increase in the proportion of excellent students. Students′ evaluation of the course has also improved. Conclusions The digital transformation of the course provides students with diversified teaching resources, stimulates their building of autonomous learning skills, and achieves significant results in course construction.

Exploration on integrating peer instruction model into the standardized residency training physician in stomatology

ZHANG Xinyuan, HUO Jingyi, YOU Pengyue, GUO Chunlan, ZHANG Xin, DONG Haitao, WAN Kuo

2026, 46(9):  1302-1306.  doi:10.16352/j.issn.1001-6325.2026.09.1302

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The peer instruction model characterized by equal collaboration and mutual learning through teaching, has increasingly demonstrated its application value in education and medicine in recent years. However, its implementation in standardized training program for dental residents remains in the exploratory phase still need accumulation of practice performance. Based on the dental resident training program at our hospital, this study systematically summarizes the application advantages, implementation pathways, and preliminary practical experience of the peer instruction model. Results of the study indicate that, as compared to classic teaching approaches, peer education model more effectively stimulates trainees′ learning initiative, enhances their in-depth understanding of theoretical knowledge, and improves proficiency in clinical operations. As a supplementary teaching model for standardized dental resident training, it holds substantial application and promotion value.