Objective To investigate the effect and mechanism of valsartan on high glucose-induced rat kidney cell proliferation and apoptosis. Methods High glucose was used to induce HBZY-1 damage in rat mesangial cells, and different concentrations of valsartan were given. Western blot detected of proliferation and apoptosis-related proteins CyclinD1, Cleaved caspase-3, Bcl-2 related X protein ( Bax), B cell lymphoma / leukemia - 2 ( Bcl-2), and NOTCH1 signaling pathway protein jagged1, NOTCH1 expression, MTT colorimetric method was performed to determine cell proliferation activity, and flow cytometry was applied to evaluate cell cycle and apoptosis. The high glucose-induced HBZY- 1 was treated with NOTCH1 signaling pathway activators Jagged 1 / Fc fusion protein and valsartan, and its effects on cell proliferation, cell cycle and apoptosis were observed. Results The expression level of CyclinD1, Bcl-2 protein, cell proliferation activity at 24 h, 48 h and 72 h, and S-phase cell ratio in HBZY-1 induced by high glucose were significantly decreased, and G0-G1-phase cell ratio, Cleaved caspase-3, Bax, jagged1 and NOTCH1 protein expression levels and apoptosis rate were greatly increased (P<0. 05). 0. 01, 0. 1, 1 μmol / L valsartan obviously improved the expression levels of CyclinD1, Bcl-2, cell proliferation activity at 24 h, 48 h and 72 h, and S-phase cell ratio, while dramatically reduced G0-G1-phase cell ratio, the expression levels of Cleaved caspase-3, Bax, jagged1, NOTCH1 and the apoptosis rate, all in a concentration-dependent manner (P<0. 05). NOTCH1 signaling pathway activator Jagged 1 / Fc fusion protein partially reversed the effects of valsartan on the proliferation, cell cycle and apoptosis of HBZY-1 treated with high glucose. Conclusions Valsartan can promote the proliferation and cell cycle of rat mesangial cells treated with high glucose by inhibiting the NOTCH1 signaling pathway, and reduce the apoptosis.