2021PubMedRequires access

Simvastatin inhibites high glucose-induced renal tubular epithelial cells apoptosis by down-regulating miR-92a.

Ying Guan, Ping Zhou, Zhangsong Sun, Lifeng Meng

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Abstract

This work aims to investigate the role of simvastatin (SIM) in renal tubular epithelial cells (HK-2) proliferation. The apoptosis model of HK-2 cells induced by high glucose was established; HK-2 cells were cultured in vitro and randomly divided into control group, model group, SIM low-dose group, SIM medium-dose group and SIM high-dose group. After 24 h culture, the inhibitory effect of SIM on high glucose- induced proliferation of HK-2 cells was evaluated by MTT method. The expression of cysteinyl aspartate specific proteinase (Caspase-3) in apoptosis-related protein was evaluated by Western blotting; miR-92a expression in HK-2 cells was measured by RT-qPCR. High glucose group had significantly lower HK-2 cell survival rate than the control group (p<0.05); SIM middle-dose and high-dose groups had higher HK-2 cell survival rate than the model group, (p<0.05); SIM low, medium and high-dose groups had lower HK-2 cell apoptosis rate, Caspase-3 protein and miR-92a expression levels than the model group (p<0.05), all showing dose-dependence.

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What this paper is about

This work aims to investigate the role of simvastatin (SIM) in renal tubular epithelial cells (HK-2) proliferation. The apoptosis model of HK-2 cells induced by high glucose was established; HK-2 cells were cultured in vitro and randomly divided into control group, model group, SIM low-dose group, SIM medium-dose group and SIM high-dose group. After 24 h culture, the inhibitory effect of SIM on high glucose- induced proliferation of HK-2 cells was evaluated by MTT method. The expression of cysteinyl aspartate specific proteinase (Caspase-3) in apoptosis-related protein was evaluated by Western blotting; miR-92a expression in HK-2 cells was measured by RT-qPCR. High glucose group had significantly lower HK-2 cell survival rate than the control group (p<0.05); SIM middle-dose and high-dose groups had higher HK-2 cell survival rate than the model group, (p<0.05); SIM low, medium and high-dose groups had lower HK-2 cell apoptosis rate, Caspase-3 protein and miR-92a expression levels than the model group (p<0.05), all showing dose-dependence.

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Available abstract

This work aims to investigate the role of simvastatin (SIM) in renal tubular epithelial cells (HK-2) proliferation. The apoptosis model of HK-2 cells induced by high glucose was established; HK-2 cells were cultured in vitro and randomly divided into control group, model group, SIM low-dose group, SIM medium-dose group and SIM high-dose group. After 24 h culture, the inhibitory effect of SIM on high glucose- induced proliferation of HK-2 cells was evaluated by MTT method. The expression of cysteinyl aspartate specific proteinase (Caspase-3) in apoptosis-related protein was evaluated by Western blotting; miR-92a expression in HK-2 cells was measured by RT-qPCR. High glucose group had significantly lower HK-2 cell survival rate than the control group (p<0.05); SIM middle-dose and high-dose groups had higher HK-2 cell survival rate than the model group, (p<0.05); SIM low, medium and high-dose groups had lower HK-2 cell apoptosis rate, Caspase-3 protein and miR-92a expression levels than the model group (p<0.05), all showing dose-dependence.

Key concepts: Simvastatin, Apoptosis, In vitro, Cell growth, Molecular biology, Blot, Caspase 3, Cell culture

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Simvastatin inhibites high glucose-induced renal tubular epithelial cells apoptosis by down-regulating miR-92a. — Research Paper | ScholarLens