Abstract: Objective To investigate the effect and possible mechanisms of angiotensin Ⅱ type 1 receptor (AT1R) on injury of renal tubular epithelial cells induced by high glucose.Methods The expression of AT1R, AdipoR1, NF-κB, MCP-1, MIP-1α, α-SMA, FN were detected by using western blot. The colocalization of AT1R and AdipoR1 was detected by confocal microscopy. The dimerization of AT1R and AdipoR1 was detected by immunoprecipitation.Results Compared with control group, the expression of AdipoR1 had no significant change and the expression of AT1R was increased in rat renal tubular epithelial cells induced by high glucose. The expression of inflammatory factors as NF-κB, MCP-1 and MIP-1α was increased in rat renal tubular epithelial cells stimulated with high glucose. Compared with control group, the expression of α-SMA and FN was increased in rat renal tubular epithelial cells stimulated with high glucose. The dimerization of AT1R and AdipoR1 was formed in the rat renal tubular epithelial cells. And the AT1R-adipoR1 dimerization was increased in the rat renal tubular epithelial cells induced by high glucose. Knockdown of AT1R by siRNA inhibited the demerization of AT1R-adipoR1, reduced the expression of inflammatory factors as NF-κB, MCP-1 and MIP-1α, decreased the expression of α-SMA and FN in rat renal tubular epithelial cells induced by high glucose.Conclusions AT1R promotes the inflammation and fibrosis of renal tubular epithelial cells induced by high glucose through dimerization of AT1R-adipoR1.