关键词: 肾素血管紧张素系统,血管紧张素转换酶2, 血管紧张素(1-7)，Mas

Abstract: Objective To investigate the effects of Ang-(1-7) and Mas receptor on insulin secretion in NIT cell and their potential mechanism. Methods NIT cells were exposed to Ang-(1-7) of different concentrations (10-8 mol/l～10-3mol/l) for 24 hours. Glucose stimulated insulin secretion by NIT cells was detected with ELISA. The full cDNA sequence of Mas, GLUT-2 and TGF-β1 were obtained from NIT cell line using RT-PCR. After NIT cells were exposed to 10-5mol/l Ang-(1-7) for 48 hours, Mas, GLUT-2 and TGF-β 1 mRNA expression were estimated by real-time PCR; Meantime, the protein levels of the afore variables were detected by Western blotting analysis. Results NIT islet cell line responds to extracellular Ang-(1-7) (10-8 mol/l -10-3mol/l) with increased insulin secretion in a concentration dependent manner. The insulin secretion increased significantly in the presence of 10?5mol/l Ang-(1-7) (8.86±0.53 mIU/l) compared to control group (8.06±0.39 mIU/l) (P<0.05). In the experiments, compared to control group, the cells preincubated with 10?5mol/l Ang-(1-7) were up-regulated in Mas gene and protein expression (P<0.05～0.01), and caused a significant stimulation of mRNA and protein expression of GLUT-2 (P<0.05). On the contrary, the result showed a reduction in TGF-β1 mRNA and protein expression (P<0.05). Conclusion The binding of Ang-(1-7) and Mas can stimulate the NIT cells to secrete insulin, probably due to its enhancing the ability to intake glucose and inhibit the progression of fibrosis.

Key words: Rennin-angiotensin system, Angiotensin-converting Enzyme 2, Angiotensin-(1-7), Mas