Table of Content

05 July 2026, Volume 46 Issue 7

Previous Issue   

Original Articles

FBXO2 is a potential tumor pattern recognition ligand of Vδ1 γδ T cells

LIU Ruiqi, ZHANG Jianmin, HE Wei, CHEN Hui

2026, 46(7):  887-894.  doi:10.16352/j.issn.1001-6325.2026.07.0887

Asbtract ( 22 )   PDF (6258KB) ( 12 )  

References | Related Articles | Metrics

Objective To validate F-box protein 2 (FBXO2) as a potential tumor-specific pattern recognition ligand for γδ T cells and to characterize its expression in tumor cells and function in immunotherapy. Methods The expression of FBXO2 in various human solid tumor and hematological tumor cell lines was detected by Western blot and flow cytometry. Immobilized FBXO2 recombinant protein was used to expand Vδ2 and Vδ1 γδ T cells from human peripheral blood mono-nuclear cell(PBMC), followed by comprehensive characterization of cellular purity, absolute counts, activation marker expression and cytokine secretion profiles. The inhibitory effect of FBXO2-specific antibody on the in vitro cytotoxicity of Vδ1and Vδ2 γδ T cells was evaluated via antibody blockade experiment. Results FBXO2 was expressed in some human solid and hematological tumor cell lines especially in the gastric cancer line SNU601 and the lymphocyte leukemia line Jurkat. Immobilized FBXO2 significantly promoted the expansion of Vδ1 γδ T cells but failed to stimulate Vδ2 γδ T cells. Vδ1 γδ T cells exerted cytotoxic activity by recognizing FBXO2 protein while FBXO2 antibody blocked their cytotoxic effects on SNU601 and Jurkat cells with a dose-dependent manner in vitro. Conclusions F-Box2 protein, ectopically expressed on a variety of tumor cell surface, may promote the expansion of Vδ1 γδ T cells and enhance the cytotoxicity of γδ T cells against tumor cells in vitro,so this protein molecule is believed to be a tumor-associated protein ligand recognized by γδ T cells. This result suggests a potential nascent target for cancer immunotherapy.

Application of theoretical spectra in spectral flow cytometry of mouse bone marrow cells

LI Zhuo, LIU Xuehui, LI Jing, FAN Hong, FAN Hualin, LYU Xiang

2026, 46(7):  895-903.  doi:10.16352/j.issn.1001-6325.2026.07.0895

Asbtract ( 19 )   PDF (7828KB) ( 7 )  

References | Related Articles | Metrics

Objective To investigate the feasibility and limitations of theoretical spectra applied as substitutes for single-stained controls in spectral flow cytometry, and to propose a reference-spectrum optimization strategy for correcting deviations between theoretical and experimentally measured spectra caused by auto-fluorescence. Methods Mouse bone marrow single-stained samples were collected and analyzed by multi-platform spectral flow cytometry. Cosine similarity was used to evaluate the consistency between theoretical spectra and experimentally measured spectra. For single-stained samples affected by autofluorescence, reference spectra were generated from cell subsets with relatively homogeneous auto-fluorescence, and their effects on performance were assessed. Results Among eleven antibody-fluorochromes/fluorescent dyes, five of them showed cosine similarity values of 0.90 or higher between measured and theoretical spectra on both platforms, which suggested that they might serve as alternatives to single-stained controls. Spectral mismatches manifested either as spectral shifts related to detection conditions or, in a subset of samples, as abnormal reference spectra associated with auto-fluorescence interference. The subset strategy corrected abnormal reference spectra caused by auto-fluorescence heterogeneity and significantly reduced unmixing spillover errors in mouse bone marrow cells. Conclusions Theoretical spectra can serve as effective tools for evaluating and correcting reference spectra and may partially replace single-stained controls. The subset strategy can reduce reference-spectrum bias caused by autofluorescence and improve the accuracy of spectral unmixing.

Construction and validation of a gemcitabine resistance gene signature based on cholangiocarcinoma organoids

CHEN Ziran, HUANG Rong, LU Yan, LI Kai, SONG Wei

2026, 46(7):  904-912.  doi:10.16352/j.issn.1001-6325.2026.07.0904

Asbtract ( 19 )   PDF (5621KB) ( 4 )  

References | Related Articles | Metrics

Objective To develop a transcriptional signature of gemcitabine (GEM) resistance using patient-derived organoids (PDOs) from cholangiocarcinoma and to validate its biological consistency and predictive relevance. Methods Transcriptomic profiles and drug sensitivity data from four PDOs were collected and analyzed through Hallmark pathway enrichment and pre-ranked GSEA in order to construct a 23-gene resistance signature. The associated pathway patterns were validated in TCGA-CHOL and GSE236894 cohorts, while correlations with drug response metrics were assessed with CCLE and PharmacoDB, complemented by experimental validation in cell models. Results GEM resistance was primarily enriched in cell cycle and E2F target pathways. The 23-gene signature was positively correlated with AUC in PDOs and significantly associated with proliferation markers (e.g., TOP2A, MKI67) and cell cycle activity in independent cohorts. Database analyses further demonstrated a significant positive correlation between the signature score and GEM AAC_recomputed (ρ=0.149, P＜0.001), with higher scores which indicated a stronger resistance. Experimental findings confirmed that signature-related genes remained expressed in resistant cells but were suppressed in sensitive cells. Conclusions This signature provides a robust and biologically interpretable indicator of GEM resistance in cholangiocarcinoma, with strong generalizability across datasets.

Pro-inflammatory functions of intestinal intraepithelial γδ T cells in mouse models of inflammatory bowel disease

XU Yi, ZHANG Siya, ZHANG Jianmin, HE Wei, CHEN Hui

2026, 46(7):  913-924.  doi:10.16352/j.issn.1001-6325.2026.07.0913

Asbtract ( 19 )   PDF (12448KB) ( 7 )  

References | Related Articles | Metrics

Objective To investigate the pro-inflammatory function and mechanisms of γδ T cells derived from intestinal intraepithelial lymphocytes (IELs) in a mouse model of inflammatory bowel disease (IBD) induced by dextran sulfate sodium (DSS). Methods Mouse model of IBD was established by DSS administration in both γδ T cell knockout (KO) mice and in wild-type (WT) mice. Intestinal tissue damage was evaluated by the disease activity index (DAI) and hematoxylin-eosin (HE) staining microscopy. Flow cytometry was employed to analyze the proportion, subset composition, cytokine secretion, and surface cluster of differentiation (CD27) expression of γδ T cells isolated from the spleen(SPL), peripheral lymph nodes(LNs) and IEL.Bulk RNA sequencing(bulk RNA-seq) was performed to examine transcriptomic changes while and immune repertoire sequencing was used to evaluate the character of TCRγδ repertoire. Results Compared to WT controls, γδ T cell KO mice exhibited lower DAI scores(P＜0.05) and milder tissue damage following DSS administration. The proportion of γδ T cells in the IEL was higher than that in the spleen or peripheral lymph nodes but significantly increased after DSS treatment(P＜0.05). The relative proportions of Vγ1 and Vγ4 subsets,IFN-γ and IL-17 secretion, and surface CD27 expression did show any significant difference between untreated and DSS-treated groups. However, bulk RNA-seq analysis revealed a down regulation of anti-bacterial molecule genes and anti-inflammatory genes in DSS-treated mice(P＜0.05).Immune repertoire analysis showed that complementarity determining region(CDR)3 diversity in γδ T cells from DSS-induced mice was reduced significantly(P＜0.05). Conclusions IEL-derived γδ T cells promote intestinal inflammation in DSS-induced colitis via mechanisms that appear independent of pro-inflammatory cytokine secretion. These cells exhibit reduced inflammation-associated CDR3 diversity, impaired anti-microbial pathway activity, and disrupted immunoregulatory signaling. The results of this research may support the development of novel therapeutic strategies for IBD.

Anti-tumor activity of a novel peptide-drug conjugate TPL-P7

WANG Runlin, WU Mo, HUANG Wei, LI Wenhua, YANG Nan, LIU Yanyong

2026, 46(7):  925-931.  doi:10.16352/j.issn.1001-6325.2026.07.0925

Asbtract ( 14 )   PDF (3599KB) ( 5 )  

References | Related Articles | Metrics

Objective To investigate the anti-tumor effect of the peptide conjugate drug TPL-P7, which is a dual-targeting Peptide 7(P7) and triptolide (TPL), and targeted at HSP90. Methods In the test system of non-small cell lung cancer cell line A549, the cell viability was evaluated by sulforhodamine B (SRB) assay after 48 hours of treatment with TPL alone or in combination with P7. Furthermore, the apoptosis was evaluated by flow cytometry to explore the synergistic effect of the targeting peptide P7 and triptolide. The anti-tumor activity of the peptide conjugate drug TPL-P7 was evaluated by SRB assay. Subsequently, an in vivo anti-tumor activity of TPL-P7 was assessed in the subcutaneous xenograft tumor model of non-small cell lung cancer cell line A549. Result TPL and P7 combination led to a significant left shift in the cell survival curve of TPL, indicating that the P7 significantly increased the sensitivity to TPL. The equivalent line graph showed that the dose ratios of P7 combined with TPL were 2∶1, 1∶1, and 1∶2, all of which were below the equivalent line, and the optimal ratio point was 1∶1. Flow cytometry results demonstrated that combination significantly promoted apoptosis, which was higher than that of the TPL single drug group (P＜0.05). TPL-P7 exhibited significant tumor-killing effects in both A549 and PANC-1 cells, with IC₅₀ values of 14.0 μmol/L and 2.8 μmol/L respectively. After four weeks of administration, the tumor inhibitory rate of TPL-P7 was as 60%, significantly different from the equal-molar dose of TPL(P＜0.05).ConclusionsThere are a synergistic killing effect of targeting peptide P7 and triptolide. The peptide conjugate drug TPL-P7 exerts an anti-tumor activity both in vitro and in vivo with low toxic side effects.

Autophagy inhibitor Spautin-1 increases apoptosis rate in human pancreatic cancer cell line PaTu 8988t

DONG Zeyao, LIN Shuyu, DAI Li

2026, 46(7):  932-938.  doi:10.16352/j.issn.1001-6325.2026.07.0932

Asbtract ( 15 )   PDF (4624KB) ( 3 )  

References | Related Articles | Metrics

Objective To investigate the effects of Spautin-1, an inhibitor of ubiquitin-specific peptidase 10 (USP10), on the proliferation, migration, autophagy, and apoptosis of human pancreatic cancer cell line PaTu 8988t, and to explore the underlying mechanisms. Methods Analysis of standardized TCGA/GTEx pancreatic ductal adenocarcinoma (PAAD) data from UCSC Xena was performed with GEPIA 2 to assess USP10 expression, its prognostic value and its potential correlation with autophagy genes (MAP1LC3B and SQSTM1). Validation and visualization were conducted with R language on the GEO dataset. PaTu 8988t cells were incubated with Spautin-1 (0~200 μmol/L). Cytotoxicity was determined by CCK-8 assay, and 20 μmol/L was selected for subsequent experiments. Cell migration and invasion were evaluated by wound healing and Transwell assays, respectively. Apoptosis was detected by flow cytometry (annexin V-FITC/PI double staining). Intracellular reactive oxygen species (ROS) level was measured with the DCFH-DA probe. Protein expression of USP10, LC3-Ⅱ and p62 was measured by Western blot. All experiments were independently repeated at least three times. Results 1)GEPIA 2 USP10 was up-regulated in PAAD accompanied by a poor prognosis/The expression was positively correlated with the autophagy genes MAP1LC3B and SQSTM1. Validation with GSE16515 dataset confirmed this expression trend, and clustering analysis suggested USP10's potential involvement in autophagy regulation. 2)Spautin-1 dose-dependently inhibited cell viability. 3)Spautin-1(20 μmol/L) significantly suppressed scratch healing rates and Transwell invasion (P＜0.05). 4)Spautin-1 down regulated LC3-Ⅱ and USP10 protein levels while up-regulating p62, indicating impaired autophagy flux(P＜0.05). 5)Spautin-1 significantly increased intracellular ROS level and apoptosis rates(P＜0.05). Conclusions Spautin-1 effectively inhibits proliferation and migration/invasion of PaTu 8988t cells. Its effects are accompanied by a reduced USP10 expression, blocked autophagy flux, ROS accumulation and increased apoptosis which suggest a potential mechanism involving USP10 inhibition, autophagy disruption and ROS-dependent apoptosis.

Taurodeoxycholic acid inhibits the high glucose-induced apoptosis of human retinal microvascular endothelial cells(hRMECs)

YANG Qian, LIU Yuan, DU Juan, MA Shengnan, LI Na, CHANG Hu, GAO Ge

2026, 46(7):  939-944.  doi:10.16352/j.issn.1001-6325.2026.07.0939

Asbtract ( 14 )   PDF (2209KB) ( 4 )  

References | Related Articles | Metrics

Objective To investigate the effect of taurodeoxycholic acid (TUDCA) in inhibiting apoptosis of human retinal microvascular endothelial cells (hRMECs) induced by high glucose (HG). Methods hRMECs were divided into control group, HG group (30 mol/L glucose induced cells for 24 hours), L-TUDCA, M-TUDCA, H-TUDCA groups (HG+1, 10, 100 μmol/L TUDCA)and TUDCA+ML385 group (HG+100 μmol/L TUDCA+5 μmol/L Nrf2 inhibitor ML385). CCK8 method was used to detect hRMECs proliferation. Transwell experiment was used to detect hRMECs migration. Flow cytometry was used to detect hRMECs apoptosis. ELISA was used to detect the level of oxidative stress factors in cell supernatant. The expression of Keap1, Nrf2, and HO-1 proteins in hRMECs was checked by Western blot. Results The A₄₅₀ value, migration number, GSH, SOD, Nrf2 and HO-1 in the HG group were all lower than those in the control group, while the apoptosis rate, ROS, MDA, and Keap1 were higher than those in the control group (P＜0.05). The A₄₅₀ value, migration number, GSH, SOD,Nrf2,and HO-1 in the L-TUDCA group, M-TUDCA group, and H-TUDCA group were higher than those in the HG group, while the apoptosis rate, ROS, MDA, and Keap1 were lower than those in the HG group (P＜0.05). The A₄₅₀ value, migration number, GSH, SOD, Nrf2, and HO-1 in the TUDCA+ML385 group were lower than those in the H-TUDCA group, while the apoptosis rate, ROS, and MDA were higher than those in the H-TUDCA group(P＜0.05). Conclusions TUDCA can inhibit HG-induced hRMECs apoptosis and Keap1-Nrf2/HO-1 signaling pathway is potentially be involved in this process.

Inflammatory injury of endometriosis tissues is related to ferroptosis

GUO Bingjing, YE Wenwei, SHI Jinmei, XIU Limeng, CHAI Zhihong, ZHU Weijun

2026, 46(7):  945-949.  doi:10.16352/j.issn.1001-6325.2026.07.0945

Asbtract ( 13 )   PDF (1041KB) ( 3 )  

References | Related Articles | Metrics

Objective To explore the correlation between inflammatory in endometriosis (EMs) tissues collected from patients and ferroptosis as well as its clinical significance. Methods From January 2021 to December 2024, 31 EMs patients who visited the gynecology department of Taizhou Municipal Hospital were selected, and 20 cases of patients with benign gynecological diseases were collected as control group.The lesion endometrium tissues and normal endometrium tissues were sampled. Pain degree of dysmenorrhea, inflammatory injury of endometrium, and ferroptosis-related mRNA/protein in the two groups were observed by HE staining microscopy, real-time PCR or Western blot. The results were statistically analyzed to evaluate the correlation among pain, inflammatory injury of endometrium, and ferroptosis. Results The pain degree of EMs group patients was mainly in the moderate to severe range, while that of the control group patients was mainly in the mild to moderate range. Compared with the control group, the endometrial tissues of the EMs group patients had obvious incomplete tissue structure with a large number of inflammatory cell infiltration. Moreover, the mRNA level of TNF-α, IL-1β, and TGF-β and the protein level of SOD, MDA and GSH in the endometrium of the EMs group patients were significantly increased(P＜0.05); Compared with the control group, the protein expression of GXP4 and CD71 in the endometrium of the EMs group patients were significantly increased (P＜0.001)and the protein expression level of HO-1 was significantly decreased (P＜0.001). Conclusions The pain degree of dysmenorrhea in EMs patients is positively correlated with the inflammatory injury of endometrium and the oxidative stress and ferroptosis in lesion endometrium were found.

ALKBH5 ameliorates renal interstitial fibrosis in mouse models with unilateral ureteral obstruction by regulating the expression of Fdx1

HOU Donghua, WU Qi, LIANG Hui, BAO Nana, LYU Huiyan, DAI Deyu, ZHANG Lei

2026, 46(7):  950-956.  doi:10.16352/j.issn.1001-6325.2026.07.0950

Asbtract ( 20 )   PDF (2263KB) ( 4 )  

References | Related Articles | Metrics

Objective To explore the effect of alkylated repair(RNA demethylase ALKB) homologue 5 (ALKBH5) to regulate the expression of cuproptosis-related gene ferredoxin 1 (Fdx1) on renal interstitial fibrosis (RIF) in unilateral ureteral obstruction (UUO) mice. Methods The UUO model mice were randomly divided into a model group (UUO group), a negative control group (LV5-vector group), an ALKBH5 over-expression group (LV5-ALKBH5 group), an LV5-vector+ FDX1 activator (Elesclomol) group and an LV5-ALKBH5+Elesclomol group, with 12 mice in each .Another 12 healthy mice were taken as control group (control group). ELISA kit was used to detect serum inflammatory factor; HE and Masson staining microscopy was used to observe renal histopathological changes and fibrosis; RT-qPCR detection of epithelial-mesenchymal transition (EMT)-related genes and Alkbh5 and Fdx1 mRNA expression in renal tissue epithelial cells; The expression of ALKBH5 and FDX1 protein were detected by immunoblotting. Results Compared with the control group, mice in the UUO group showed increased renal tissue lesions, increased percentage of fibrosis (P＜0.05), increased serum renal function indexes; Higher level of inflammation factor and renal tissue α-SMA, snail and FDX1 expression (P＜0.05), and decreased E-cadherin and ALKBH5 expression (P＜0.05).Compared with the LV5-vector group, mice in the LV5-ALKBH5 group showed significantly improved results on above indexes (P＜0.05). Over-expression of ALKBH5 was reversed which promoted FDX1 activation on renal tissue inflammation, EMT and renal interstitial fibrosis in UUO mice. Conclusions ALKBH5 may attenuate the inflammatory response, inhibit EMT, ameliorate kidney injury, and alleviate RIF in UUO mice by down-regulating the expression of the cuproptosis-related gene Fdx1.

Murine pancreatic cancer cell line Pan02-derived exosomes effectively improve motor dysfunction in mouse models of Parkinson's disease

ZHANG Kexin, XIAO Fangyan, LI Wenhua, HUANG Wei, LIU Yanyong, YANG Nan

2026, 46(7):  957-964.  doi:10.16352/j.issn.1001-6325.2026.07.0957

Asbtract ( 16 )   PDF (3138KB) ( 2 )  

References | Related Articles | Metrics

Objective To investigate the therapeutic effects of murine pancreatic cancer cell line Pan02l-derived exosomes(Exos) on Parkinson's disease (PD) in a mouse model. Methods Pan02 cell-derived exosomes were extracted by commercially available kit and then characterized by transmission electron microscape(TEM), nanoparticle tracking analysis and Western blot. In vitro, the protective effect of exosomes on a mouse model of 1-methyl-4-phenylpyridinium (MPP⁺)-induced MN9D dopaminergic neuron injury was detected by CCK-8 assay. A C57BL/6J mice of acute 1-methyl-4-phenyl-1,2, 3, 6-tetrahydropyridine (MPTP)-induced PD was established. The mice were divided into a wild-type (WT) control group, a PD model group, and low, medium, and high-dose exosome groups (Exo-L, Exo-M, Exo-H). Exosomes were administered via multiple tail vein injections. Motor function and neurobehavioral changes were assessed using the balance beam test, pole test, rotarod test, open field test and Y-maze test. Damage to dopaminergic neurons in the substantia nigra and striatum was evaluated by immunofluorescence microscopy. A tumor-bearing mouse model was also established for a preliminary safety evaluation. Results Exosomes markedly reversed the MPP⁺-induced decrease in MN9D cell viability (P＜0.001). Compared with the PD model group, the Exo-L group showed a substantial reduction in beam crossing time (P＜0.001) and pole descent time (P＜0.05). The Exo-M group exhibited a significant decrease in total distance moved in the open field test (P＜0.05). No notable differences were observed in anxiety and cognition-related behavioral parameters among all groups. Exosomes dramatically mitigated MPTP-induced loss of tyrosine hydroxylase (TH)-positive neurons in the substantia nigra (Exo-L group, P＜0.05; Exo-H group, P＜0.01) and reduction of TH-positive fiber density in the striatum (Exo-L and Exo-M groups, P＜0.05). Safety evaluation confirmed that exosomes did not promote tumor growth in tumor-bearing mice. Conclusions Pan02 cell-derived exosomes effectively alleviate MPP⁺/MPTP-induced dopaminergic neuron injury, ameliorate motor dysfunction in PD mouse models, and exhibit no tumor-promoting risk, demonstrating favorable neuro-protective effects and safety.

Establishment of KRAS G12C-mutant pancreatic cancer cell strains with stable Cas9 expression and differential sensitivity to targeted KRAS inhibitors

WU Yani, DAI Jiayin, YANG Zhenli, HOU Yuhong, BIAN Xiaocui, LIU Yuqin

2026, 46(7):  965-974.  doi:10.16352/j.issn.1001-6325.2026.07.0965

Asbtract ( 17 )   PDF (6005KB) ( 4 )  

References | Related Articles | Metrics

Objective To establish a human pancreatic cancer cell line harboring a Kirsten rat sarcoma viral proto-oncogene (KRAS) G12C mutation and to construct isogenic single-cell clonal strains with stable Cas9 expression, thereby to provide a standardized cellular model for the study of targeted therapy resistance of pancreatic cancer. Methods Cells were isolated from surgically resected tumor tissue of a pancreatic cancer patient and subjected to primary culture and serial passaging to establish a stable cell line. Systematic characterization was performed through morphological observation, short tandem repeat (STR) profiling, mycoplasma testing, subcutaneous tumor formation in NOD/SCID mice, histopathological analysis, and whole-exome sequencing (WES). A Cas9-stably expressing cell line was subsequently constructed, and single-cell clones were screened. The half-maximal inhibitory concentration (IC₅₀) of each clone against sotorasib and RMC-6236 was determined by CCK-8 assay. RNA sequencing(RNA-seq) combined with gene set enrichment analysis (GSEA) was employed to evaluate signaling pathways associated with differential drug sensitivity. Results A human pancreatic cancer cell line, designated PUMC-PAAD7, and was successfully established. The cell line was continuously passaged for more than 40 times in vitro, formed subcutaneous xenograft tumors in NOD/SCID mice, which exhibited histopathological features consistent with pancreatic cancer and harbored a KRAS G12C mutation. Seven isogenic Cas9-stably expressing single-cell clones were obtained, among which PUMC-PAAD7-C6 and PUMC-PAAD7-C7 displayed marked drug sensitivity heterogeneity. C6 was highly sensitive to both inhibitors, whereas C7 exhibited prominent resistance, with IC₅₀ values 16-fold and 23-fold higher than those of C6, respectively. RNA-seq identified 362 differentially expressed genes. GSEA revealed significant enrichment differences between the two clones in the NF-κB signaling, sphingolipid signaling and podosome assembly pathways. Conclusions A KRAS G12C-mutant pancreatic cancer cell line is successfully established. And seven isogenic Cas9-stably expressing single-cell clonal strains are constructed. These strains exhibit intrinsic drug sensitivity heterogeneity, provide an ideal isogenic paired model for investigating the mechanisms underlying primary resistance to KRAS inhibitors.

Shumian capsule alleviates learning and memory impairment caused by chronic sleep deprivation in mouse models

HAN Songyan, LI Wenhua, ZHAO Haiqing, YAN Yan, LIU Yanyong, YANG Nan

2026, 46(7):  975-981.  doi:10.16352/j.issn.1001-6325.2026.07.0975

Asbtract ( 13 )   PDF (3022KB) ( 2 )  

References | Related Articles | Metrics

Objective To investigate the effect of Shumian capsule (SMC) on learning and memory impairment induced by chronic sleep deprivation and to explore its underlying mechanism. Methods A chronic sleep deprivation (CSD) model was established with a modified multiple platform method (MMPM). The pentobarbital sodium sleep test, Barnes maze test, open field test (OFT), and forced swimming test (FST) were conducted for behavioral analysis. Western blot was used to detect the expression level of alpha2A-adrenergic receptor (α2A-AR), TWIK- related potassium channel 2(TREK2),and protein kinase A (PKA) catalytic subunit. Results Compared with the model group, high-dose SMC significantly reduced sleep onset latency (P＜0.05); low-, medium-, and high-dose SMC all significantly prolonged sleep time (L-SMC, M-SMC, and H-SMC groups, P＜0.001). In the Barnes maze test, after three consecutive days of training, CSD mice showed a significantly increased latency to find the target hole (P＜0.001). Treatment with medium- and high-dose SMC significantly reduced the latency, with the most pronounced effect observed in the high-dose SMC group (P＜0.001). In the open field test (OFT), the time spent in the center zone was significantly increased in CSD mice (P＜0.001), while all SMC-treated groups showed significantly reduced center zone time (L-SMC group, P＜0.05; M-SMC group, P＜0.01; H-SMC group, P＜0.001). In forced swimming test (FST), used to assess depressive-like behavior, the immobility time was significantly reduced in the high-dose SMC group compared with the model group (P＜0.001). In the prefrontal cortex of CSD mice, the protein levels of α2A-AR and TREK2 were significantly increased (P＜0.05)and SMC treatment reversed this increase. Conclusions SMC might improve learning and memory impairment by inhibiting α2A-AR/TREK2 channel-mediated hyper polarization of cortical neurons. SMC alleviates sleep disturbances and learning and memory impairments. High-dose SMC exhibits the most significant effect in improving learning and memory impairment. SMC may enhance learning and memory by modulating neuronal excitability via the inhibition of the α2A-AR/TREK2 pathway.

AU-rich elements(AREs) and their binding proteins coordinate developmental programs

XIN Mingjun, HUO Yue, WANG Fang

2026, 46(7):  982-989.  doi:10.16352/j.issn.1001-6325.2026.07.0982

Asbtract ( 14 )   PDF (3760KB) ( 3 )  

References | Related Articles | Metrics

Objective To explore the potential synergistic roles of AU-rich elements (AREs) and their binding proteins (AREBPs) in post-transcriptional regulation and the translation process. Methods A customized algorithm was utilized to extract the core ARE motifs within the 3'UTR regions across human and mouse genomes.The binding sites of AREBPs were identified by integrating data from the Postar3 database, public CLIP-seq datasets from GEO.Independently constructed CLIP-seq database and PrismNet deep learning predictions. Fisher's exact test was applied to calculate the enrichment degree (odds ratio) of specific AREBPs in tissue-specific genes.The co-expression patterns between AREBPs and target genes were analyzed by combining the GTEx database and tissue-specific developmental RNA-seq datasets (e.g., kidney development dataset GSE100859). Results A comprehensive genome-wide map of conserved 3'UTR AREs in humans and mice was successfully generated.Specific AREBPs exhibited significant binding enrichment (P＜0.05) in tissue-specific genes associated with muscle, brain, kidney and heart.Expression profiling analysis revealed that during tissue development (such as kidney development), genes containing AREs showed significantly different expression patterns compared to those without AREs. Conclusions AREs and their binding proteins play a highly specific function in kidney development, genes containing AREs showed significantly different expression patterns as compared to those without AREs. Conclusions AREs and their binding proteins play a highly specific role in post-transcriptional regulation across different tissues. This study provides a crucial bioinformatics evidence for understanding the RNA regulatory mechanisms underlying tissue development and homeostasis maintenance.

Clinical Sciences

Choroidal vascular characteristics is associated with retinal nerve fiber layer thickness in ocular hypertension and primary open-angle glaucoma

WANG Xiaolei, MENG Zhaoyang

2026, 46(7):  990-997.  doi:10.16352/j.issn.1001-6325.2026.07.0990

Asbtract ( 18 )   PDF (2075KB) ( 3 )  

References | Related Articles | Metrics

Objective To compare the correlation between choroidal vascular parameters and retinal nerve fiber layer(RNFL) thickness in ocular hypertension(OHT) and primary open-angle glaucoma(POAG) using wide-field optical coherence tomography angiography(WF-OCTA) . Methods This single-center, retrospective cross-sectional study included 30 patients who underwent WF-OCTA examination at Beijing Friendship Hospital from January to December 2025. Participants were divided into normal control, OHT and POAG groups with 10 in each. WF-OCTA was used to measure choroidal vascular volume (CVV), choroidal vascular index (CVI) and RNFL thickness in concentric annular regions centered on the fovea (1-6 mm, 6-12 mm, 12-15 mm, 15-18 mm, 18-21 mm). The Kruskal-Wallis test compared group differences. Multiple linear regression analyzed associations between group CVV, CVI, and RNFL thickness, adjusting for age, gender, axial length (AL) and intraocular pressure (IOP) before and after treatment. Interaction effects were tested. Results Significant differences were observed among groups in age, disease duration, number of medications, central corneal thickness and IOP before and after treatment(P＜0.05). Compared with controls, the POAG group showed significantly thinner RNFL thickness and lower CVV in multiple peripheral regions, with higher CVI in some areas (P=0.045). Compared with controls, the OHT group showed no significant RNFL difference but had lower CVV and higher CVI in some regions. After adjustment, post-treatment IOP and axial length were independently negatively correlated with RNFL thickness in multiple regions(P＜0.05). In the central 1-6 mm region, CVI was positively correlated with RNFL thickness(β=448.79,P=0.011),with a significant group-CVI interaction(P＜0.05),indicating attenuated CVI influence on RNFL in OHT and POAG groups. Conclusions WF-OCTA demonstrates that the CVI (particularly in the central 1-6 mm region) is more significant than the CVV, showing a positive correlation with RNFL thickness, which is modulated by disease status. Post-treatment intraocular pressure and axial length are the core factors affecting RNFL thickness.

Association between baseline nutritional status and chronic radiotherapy-induced adverse effects

ZHEN Hongnan, WANG Fang, XIAO Jianing, JIANG Fei, ZHANG Yuan, SHEN Jing

2026, 46(7):  998-1003.  doi:10.16352/j.issn.1001-6325.2026.07.0998

Asbtract ( 12 )   PDF (774KB) ( 2 )  

References | Related Articles | Metrics

Objective To investigate the relationship between baseline nutritional status and chronic radiotherapy-induced adverse effects in cervical cancer patients after radiotherapy. Methods A total of 109 previously untreated cervical cancer patients undergoing definitive concurrent chemoradiotherapy were prospectively enrolled. Baseline nutritional status was evaluated by Nutritional Risk Screening 2002( NRS 2002),body mass index(BMI), skeletal muscle index, body fat percentage and visceral fat area. The incidence and severity of chronic radiation enteritis, cystitis and hematological toxicity were recorded during follow-up. Univariate and multivariate Logistic regression were used for statistical analysis. Results The incidence of chronic radiation enteritis, cystitis and hematological toxicity was 37.6%, 24.8% and 42.2%, respectively. Baseline nutritional risk was an independent risk factor for chronic radiation enteritis (OR=2.77, 95% CI: 1.19-6.42, P=0.016). Higher NRS scores were associated with chronic hematological toxicity. No significant correlation was found between nutritional indicators and radiation cystitis. BMI, wasting and low muscle mass were not independently associated with chronic adverse effects. Conclusions Baseline nutritional risk and elevated NRS scores significantly increase the risk of chronic radiation enteritis and hematological toxicity in cervical cancer patients after radiotherapy. Routine nutritional screening and early intervention before radiotherapy may reduce long-term chronic radiation injury.

Mini Reviews

Research progress in the role of NLRP3 inflammasome in hepatic ischemia-reperfusion injury

LIU Cuiling, YU Shuna

2026, 46(7):  1004-1008.  doi:10.16352/j.issn.1001-6325.2026.07.1004

Asbtract ( 15 )   PDF (415KB) ( 12 )  

References | Related Articles | Metrics

Hepatic ischemia-reperfusion injury (HI/RI) is an inevitable pathophysiological process in liver surgery and is an important factor leading to severe postoperative complications. Its mechanism is complex, involving multiple pathways such as oxidative stress, intracellular calcium overload, and inflammatory response. In recent years, as an important regulatory hub of the innate immune response, the NOD-like receptor thermal protein domain associated protein 3(NLRP3) inflammasome has played a core role in HI/RI. This article reviews the structure and function of the NLRP3 inflammasome, its activation mechanism in HI/RI to identify the core role of this molecule and to explore the research status and challenges of various intervention strategies targeting NLRP3, providing new theoretical perspectives and orientation for clinical prevention and treatment of HI/RI.

Research progress in the regulatory mechanism of tumor-associated intronic enhancer region SNPs

LI Xianqun, CHI Yuxin, MIAO Jiaming, QI Xiaolu, WEI Tong, YANG Weihong

2026, 46(7):  1009-1013.  doi:10.16352/j.issn.1001-6325.2026.07.1009

Asbtract ( 14 )   PDF (353KB) ( 3 )  

References | Related Articles | Metrics

single nucleotide polymorphisms(SNPs) are the most common genetic polymorphisms. Intronic enhancer region SNPs(IER-SNPs) can influence the progress of carcinomaigenesis and progression of breast cancer, colorectal cancer, lung cancer and other carcinomas by multiple approaches including influencing the transcription factor binding,promoter-enhancer interactions and mediating the enhancer-promoter switching effect and so on. By sorting out the regulatory mechanisms of IER-SNPs on tumors, it can provide references for screening tumor-associated IER-SNPs formation and development and or research on regulatory mechanisms of these IER-SNPs.

Mechanism of irisin effect in type 2 diabetes mellitus and chronic heart failure

YANG Xue, CHENG Xiaoliang

2026, 46(7):  1014-1018.  doi:10.16352/j.issn.1001-6325.2026.07.1014

Asbtract ( 12 )   PDF (439KB) ( 3 )  

References | Related Articles | Metrics

Type 2 diabetes mellitus(T2DM) is closely related to chronic heart failure in the view point of patho-physiological mechanism. Research has shown that irisin as a muscle factor induced by exercise, is widely distributed in human body, which may improve blood glucose threshold of T2DM through a mechanism of reducing insulin resistance, regulating glucose and lipid metabolism, protecting beta cell function, and enhancing cardiac stem cell proliferation and angiogenesis, improving cardiac pathological remodeling, reducing cell apoptosis and so to protect and improve cardiac function.

Medical Education

Practice of integrating medical humanistic education into communication scenario simulation training in the process of learning urology

DONG Jie, ZHOU Jingmin, JI Zhigang, WEI Mengchao

2026, 46(7):  1019-1022.  doi:10.16352/j.issn.1001-6325.2026.07.1019

Asbtract ( 17 )   PDF (354KB) ( 16 )  

References | Related Articles | Metrics

Objective To explore the effectiveness of integrating medical humanistic education into communication scenario simulation training in the urology ward for standardized residency training. Methods From October to December 2025, 30 resident physicians undergoing standardized training in the Urology Department of Peking Union Medical College Hospital were selected as the study subjects. Medical humanistic education was integrated into the communication scenario simulation training in the urology ward. The patient-physician communication skills were evaluated with the SEGUE framework, by standard patients before and after the training. Additionally, residents' satisfaction with the medical humanistic education was also evaluated after the training. Results After the communication training, the trainees' scores in gathering patients' information, understanding the patient and total SEGUE score were significantly higher than those before the training (P＜0.05). The evaluations by standard patients for the residents' communication competence, including conversational skills, adaptability, content of conversation, humanistic care and conversation effectiveness were also significantly higher after the training (P＜0.05). Overall satisfaction with the medical humanistic education was high after the training. Satisfaction ratings exceeded 90% in dimensions such as learning interest, national identity and societal responsibility and humanistic literacy. Satisfaction with research integrity was 83.3%, and with innovative 76.7%trainees believed the training encouraged their innovative spirit. Conclusions Integrating medical humanistic education into communication scenario simulation training in urology ward may enhance the patient-physician communication skills of resident physicians and achieve the teaching goal of “1+1＞2” for the program of medical humanistic education.

A survey on the channels for professional knowledge acquisition among standardized residency training physician in stomatology

LIU Yuebo, GUO Chunlan, LI Zhen, WAN Kuo, DONG Haitao

2026, 46(7):  1023-1026.  doi:10.16352/j.issn.1001-6325.2026.07.1023

Asbtract ( 12 )   PDF (315KB) ( 8 )  

References | Related Articles | Metrics

Objective To investigate the pathway to achieve training outcomes of standardized training at Stomatology department, Peking Union Medical College Hospital, and to explore differences in training pathways for trainees with different training experience and educational backgrounds. Methods A questionnaire survey was conducted among 23 resident physician trainees who joined the standardized training program for stomatology, for assessing the frequency of practice and effectiveness of knowledge acquisition. Independent sample t-tests were used for inter-group comparisons. Results Overall, digital and online resources were acknowdged to be the most frequently used (4.17±0.36), while mentoring and peer guidance received the highest effectiveness ratings (4.28±0.47). The short-experience group reported significantly higher frequency of use and effectiveness ratings for “formal in-hospital training” and “mentoring and peer guidance” as compared to the long-experience group (P＜0.05). However, the long-experience group showed significantly higher application frequency of “digital and online resources” and “traditional paper-based resources” (P＜0.05). Resident physicians with postgraduate education used digital resources more frequently than those with undergraduate education or below (P＜0.05). Conclusions Resident physicians in program of stomatology standardized training have adapted diverse knowledge acquisition pathways, and their application patterns evolve with increasing experience-shifting from reliance on structured training and interpersonal guidance to active self-directed application of digital and traditional resources. Differences in the frequency of digital resource use are also observed among physicians with different educational backgrounds. The results of this investigation may support optimization of the standardized training training system and stratified implementation of training strategy.