Role of SIRT2 in LPS induced acute kidney injury in mice
韩琦 1杨焕民 1李士泽 1徐彬 1逯静静 1邢琬群 1张旭1
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作者信息
1. 黑龙江八一农垦大学动物科技学院,黑龙江大庆 163319
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摘要
Sirtuin2(SIRT2)是一种依赖NAD+的组蛋白去乙酰化酶,在维持细胞氧化还原电位方面起着关键作用,并调节促炎免疫反应.然而,其在急性肾损伤(acute kidney injury,AKI)中的作用尚未得到证实.为探究SIRT2在AKI中的作用,通过注射脂多糖(lipopolysaccharides,LPS)在野生型(WT)和SIRT2敲除(SIRT2-/-)小鼠上分别构建AKI模型.血液生化检测结果显示,与LPS处理的WT小鼠相比,SIRT2-/-小鼠肌酐和尿素氮水平更高;HE结果显示,与LPS处理的 WT小鼠相比,SIRT2-/-小鼠肾脏损伤更显著;qRT-PCR和 Western blot结果显示,炎症基因、蛋白和氧化应激蛋白在SIRT2-/-小鼠上变化的更显著.结果表明,SIRT2缺失会加重LPS诱导的AKI.
Abstract
Sirtuin2(SIRT2)is an NAD+dependent histone deacetylase that plays a key role in maintaining cellular REDOX potential and modulating pro-inflammatory immune responses.How-ever,its role in acute kidney injury(AKI)has not been proven.To explore the role of SIRT2 in AKI,AKI models were constructed in wild-type(WT)and SIRT2 knockout(SIRT2-/-)mice by injection of lipopolysaccharide(LPS).HE results showed that kidney damage in SIRT2-/-mice was more significant than that in LPS treated WT mice.qRT-PCR and Western blot results showed that more significant changes in inflammatory genes,proteins and oxidative stress proteins in SIRT2-/-mice.The results suggest that SIRT2 deficiency exacerbates LPS induced AKI.
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