Abstract: Objective To explore the effect of apigenin on human renal tubular epithelial cell damage induced by high glucose(HG) and examine whether its molecular mechanism is correlated with lncRNA MEG8. Methods Renal tubular epithelial cells HK-2 were divided into the groups of normal (NG), HG, apigenin low/medium/high-dose, HG+si-NC, HG+si-MEG8, HG+apigenin+pcDNA and HG+apigenin+pcDNA-MEG8. Real-time fluorescent quantitative polymerase chain reaction (RTqPCR) was employed for detecting the expression level of lncRNA MEG8;flow cytometry for examining cell apoptosis;Western blot for measuring protein expression;assay kits for detecting cellular superoxide dismutase(SOD) activity and malondialdehyde(MDA) content. Results In HG-induced HK-2 cells, the expression levels of MEG8, Bax and MDA were up-regulated, cell apoptotic rate rose while Bcl-2 and SOD were down-regulated(P<0. 05). After treatment with different doses of apigenin, MEG8, Bax and MDA declined, cell apoptotic rate dropped and while Bcl-2 and SOD were up-regulated in a dosedependent manner(P<0. 05). Interfering with MEG8 expression reduced apoptotic rate and MDA content induced by HG and boosted SOD activity. Overexpression of MEG8 reversed the effect of apigenin on HK-2 injury induced by HG. Conclusion Apigenin may suppress the injury of human renal tubular epithelial cells induced by HG by down-regulating the expression of lncRNA MEG8.