【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。更多还原

【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.However, 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.更多还原