Abstract: Objective To investigate the effect of miR-660-5p on high glucose-induced glomerular mesangial cell injury by regulating P53. Methods SV40-MES-13 cells were divided into two groups: control group and high glucose group, to analyze the effect of high glucose on cell viability and expression of miR-660-5p / P53. Then SV40-MES-13 cells treated with high glucose were divided into four groups: miR NC group, miR-660-5p mimic group, siNC group and siP53 group. The expression levels of miR-660-5p and P53 in SV40-MES-13 cells were detected by real-time fluorescence quantitative PCR. The growth ability of SV40-MES-13 cells was analyzed by methyl thiazolyl tetrazolium (MTT) assay. The apoptosis rate of SV40-MES-13 cells was analyzed by TUNEL and flow cytometry. Targetscan and luciferase reporter assay were used to analyze the targeting relationship between miR-660-5p and P53 in SV40-MES-13 cells. The expression level of P53 protein wasanalyzed by Western blotting. Results Compared with cells in the control group, SV40-MES-13cells treated with high glucose showed decreased proliferation activity, increased apoptosis rate, decreased expression level of miR-660-5p and increased expression level of P53. The proliferation activity of SV40-MES-13 cells treated with miR-660-5p mimic was increased, and the apoptosis rate was decreased when compared with those in the miR-660-5p NC group. The proliferation activity of SV40-MES-13 cells treated with siP53 was increased, and the apoptosis rate was decreased when compared with those in the siNC group. miR-660-5p could bind with P53 and inhibit the expressionof P53. Conclusion The expression level of miR-660-5p is decreased and the expression level ofP53 is increased in high glucose-treated mesangial cells. Up-regulation of miR-660-5p expression in high glucose-treated mesangial cells increases the proliferation activity and decreases the apoptosis rate, and the effect of miR-660-5p is related to the inhibition of P53 expression.

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