动物造模 z-bio 2022-02-12 531

　　Objective To investigate the effect and mechanism of valsartan on the proliferation and apoptosis of rat renal cells induced by high glucose.

　　Methods Rat glomerular mesangial cell HBZY-1 injury was induced by high glucose, and different concentrations of epilepsartan were administered. Western blot detection of proliferation and apoptosis-related proteins cyclin D1 (CyclinD1), activated caspase-3 (Cleaved caspase-3), Bel-2-related X protein (Bax), B cell lymphocytes The expression of tumor/leukemia-2 (Bcl-2) and NOTCH1 signaling pathway proteins jagged1 and NOTCH1, the cell proliferation activity was determined by thiazolyl blue (MTT) colorimetric method, and the cell cycle and apoptosis were evaluated by flow cytometry. High glucose-induced HBZY-1 was treated with NOTCH1 signaling pathway activator Jagged 1/Fc fusion protein and valsartan, and its effects on cell proliferation, cycle and apoptosis were observed.

　　Results The protein expression levels of CyclinD1 and Bcl-2 in HBZY-1 induced by high glucose, cell proliferation activity at 24 h, 48 h and 72 h, and the proportion of cells in S phase were significantly decreased. The protein expression levels of Bax, jagged1 and NOTCH1 and the apoptosis rate were significantly increased ( P<0.05). 0.01, 0.1, and 1 μmol/L reelsartan significantly increased the protein expression levels of CyclinD1 and Bcl-2, the cell proliferation activity at 24 h, 48 h, and 72 h, and the proportion of cells in S phase, and significantly decreased the proportion of cells in G0-G1 phase, and the proportion of Cleaved The expression levels of caspase-3, Bax, jagged1, NOTCH1 were concentration-dependent with the apoptosis rate (P<0.05). The NOTCH1 signaling pathway activator Jaged 1/Fc fusion protein partially reverses the effects of valsartan on the proliferation, cycle and apoptosis of high glucose-treated HBZY-1.

　　Conclusion Valsartan can promote the proliferation and cycle of glomerular mesangial cells in rats treated with high glucose by inhibiting NOTCH1 signaling pathway, and reduce apoptosis.