脓毒症所致肾损伤后,一般控制非抑制2促进M2巨噬细胞极化和肾功能

IF 2.9 4区 医学 Q1 Medicine
Hongfei Wang, Zhu Lin, Wenhua Li, Lin Dou
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引用次数: 0

摘要

炎性M1巨噬细胞向M2巨噬细胞的早期转移是巨噬细胞发挥抗炎作用的早期标志,而巨噬细胞在脓毒症所致肾损伤中的作用尚不清楚。我们在几个时间点用脓毒症血清治疗BMDMs,然后检测GCN2在BMDMs中的表达。Western blot检测巨噬细胞iNos和Arg1的表达。ELISA法检测炎症因子。在体内建立脓毒性肾损伤小鼠模型,采用免疫组化方法检测M1、M2标记物及IL-6水平。检测BUN、Scr、NAG评价肾功能。GCN2蛋白表达在脓毒症血清刺激的BMDMs中升高。WB结果显示,GCN2促进巨噬细胞M1向M2极化,减轻体外炎症反应。GCN2在脓毒症引起的肾损伤中表达升高。当我们过表达GCN2时,M1向M2极化增多,炎症减少,对肾功能有改善作用。我们的研究证实GCN2表达增加可以驱动M1巨噬细胞向M2极化,减轻LPS诱导的肾脏炎症,改善肾功能。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
General Control Nonderepressible 2 Promotes M2 Macrophages Polarization and Renal Function After Sepsis-Induced Renal Injury
The early metastasis of inflammatory M1 macrophages to M2 macrophages is an early marker for macrophages to play an anti-inflammatory role, while the role of macrophages in the kidney injury induced by sepsis is still poorly studied. We used septic serum to treat BMDMs at several time points, and then detect the expression of GCN2 in BMDMs. Western blot was used to detect the expression of iNos and Arg1 of macrophages. ELISA was used to detect the inflammatory cytokines. In vivo , the mice model of septic renal injury was established and immunohistochemistry was used to detect M1 and M2 markers, and IL-6 level. BUN, Scr and NAG were detected to assess renal function. The protein expression of GCN2 was increased in septic serum-stimulated BMDMs. WB results showed that GCN2 promote macrophage M1 to M2 polarization and decrease inflammation in vitro . GCN2 expression was increased in response to sepsis induced renal injury In vivo . When we overexpressed GCN2, there were more M1 polarizing to M2 and less inflammation, and it will improve renal function. Our study confirmed that increasing GCN2 expression can drive the polarization of M1 macrophages to M2, alleviate the renal inflammation and improve renal function induced by LPS.
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来源期刊
CiteScore
4.30
自引率
17.20%
发文量
145
审稿时长
2.3 months
期刊介绍: Information not localized
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