【Animal Modeling】-The Intervention Effect of Valsartan on High Glucose Induced Viability of Rat Glomerular Mesangial Cells

  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 to produce different concentrations of episaltan. Westernblot expresses the proliferation and apoptosis-related protein Cyclin D1 (CyclinD1), activated aspartate-specific caspase-3 (Cleavedcaspase-3), Bel-2 related X protein (Bax), B-cell lymphoma/leukemia- 2 (Bcl) -2) and OTCH1 signaling pathway proteins jagged1 and OTCH1, thiazole blue (MTT) colorimetric method to measure cell proliferation activity, flow cytometry to evaluate cell cycle and apoptosis. The NOTCH1 signaling pathway activator Jagged1/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: Cyclin D1, high glucose-induced HBZY-1 and Bcl-2 protein expression levels, cell proliferation activity at 24 hours, 48 hours, and 72 hours, the proportion of S phase cells was significantly reduced, the proportion of GO? G1 phase cells, Cleavedcaspuse-3, The expression level and proliferation rate of Bax, jagged1 and NOTCH1 proteins all increased significantly (Pu003c0.05). 0.01, 0.1, 1 μmol/L sartan significantly increased the expression levels of Cyclin D1, Bcl-2 protein, cell proliferation activity at 24 hours, 48 hours, and 72 hours, as well as the proportion of S phase cells. G0?. Significantly reduced G1 cells Proportion. Phase, Cleavedcaspase-3, Bax, Jagged1, NOTCH1 protein expression levels and cell apoptosis rate were all concentration-dependent (Pu003c0.05). The OTCH1 signaling pathway activator Jaged1/Fc fusion protein partially reversed the effect of valsartan on the growth, cycle and apoptosis of HBZY-1 treated with high glucose.

  Conclusion: Valsartan promotes the proliferation and circulation of rat glomerular mesangial cells treated with hyperglycemia by inhibiting the NOTCH1 signaling pathway, and reduces cell apoptosis.