动物造模 z-bio 2021-09-23 339

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

　　Method Use high glucose to induce HBZY-1 damage of rat glomerular mesangial cells, and give different concentrations of episartan. Western blot detection of proliferation and apoptosis-related protein Cyclin D1 (CyclinD1), activated aspartate-specific caspase-3 (Cleaved caspase-3), Bel-2 related X protein (Bax), B cell lymph Tumor/leukemia-2 (Bcl-2) and NOTCH1 signaling pathway protein jagged1 and NOTCH1 expression, thiazole blue (MTT) colorimetric method to determine cell proliferation activity, flow cytometry to evaluate cell cycle and apoptosis. The NOTCH1 signaling pathway activator Jagged 1/Fc fusion protein and valsartan were used to treat HBZY-1 induced by high glucose, and its effects on cell proliferation, cycle and apoptosis were observed.

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

　　Conclusion Valsartan promotes the proliferation and cycle of rat glomerular mesangial cells treated with high glucose by inhibiting the NOTCH1 signaling pathway, and reduces cell apoptosis.