Effect of Ulinastatin against human renal tubular epithelial cell injury induced by gentamicin
YE Tingting1 SHEN Jianming1 DENG Yanyan1 LIU Huihui1 YUAN Shenping2
1.Department of Nephrology, Renmin Hospital of Shiyan (People′s Hospital Affiliated to Hubei University of Medicine), Hubei Province, Shiyan 442000, China; 2.Department of Nephrology, Yunxi People′s Hospital, Hubei Province, Yunxi 442600, China
Abstract:Objective To explore the effect of Ulinastatin (UTI) against human renal tubular epithelial cells (HK-2) injury and the probable mechanism by Gentamicin-induced. Methods HK-2 were cultured in vitro and divided into Sham group, Control group, UTI group A, B and C. Sham group does nothing, Control group and UTI group were added to Gentamicin, moreover UTI group were respectively added to different doses of UTI. The cell proliferation ability, the content of lactate dehydrogenase (LDH) and malondialdehyde (MDA), the activity of superoxide dismutase (SOD), the level of vascular cell adhesion molecule (VCAM)-1, monocyte chemoattractant protein (MCP)-1, tumor necrosis factor (TNF)-α, apoptosis rate, the express of Bcl-2 mRNA and Bax mRNA were detected. Results The cell proliferation ability and the activity of SOD in Control group were lower than those in Sham group, while the content of LDH and MDA, the levels of VCAM-1, MCP-1 and TNF-α in Control group were higher than those in Sham group, moreover apoptosis rate, and the express of Bcl-2 mRNA and Bax mRNA in Control group were higher than those in Sham group, and the differences were statistically significant (P < 0.05). The cell proliferation ability and the activity of SOD in UTI groups were higher than those in Control group, and the contents of LDH and MDA, the levels of VCAM-1, MCP-1 and TNF-α in UTI groups were lower than those in Control group, while apoptosis rate, and the expression of Bax mRNA in UTI groups were lower than those in Control group, and the expression of Bcl-2 mRNA in UTI groups was higher than that in Control group, and the differences were statistically significant (P < 0.05). Furthermore, there was a dose-response relationship (P < 0.05). Conclusion UTI can reduce Gentamicin-induced HK-2 injury by reducing oxidative stress, antagonizing inflammatory responses and inhibiting apoptosis.
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