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SS-31 inhibits the inflammatory response by increasing ATG5 and promoting autophagy in lipopolysaccharide-stimulated HepG2 cells
Biochemical and Biophysical Research Communications ( IF 3.1 ) Pub Date : 2024-04-04 , DOI: 10.1016/j.bbrc.2024.149887
Yunan Mo , Songyun Deng , Yuhang Ai , Wenchao Li

SS-31 is a mitochondria-targeting short peptide. Recent studies have indicated its hepatoprotective effects. In our study, we investigated the impact of SS-31 on LPS-induced autophagy in HepG2 cells. The results obtained from a dual-fluorescence autophagy detection system revealed that SS-31 promotes the formation of autolysosomes and autophagosomes, thereby facilitating autophagic flux to a certain degree. Additionally, both ELISA and qPCR analyses provided further evidence that SS-31 safeguards HepG2 cells against inflammatory responses triggered by LPS through ATG5-dependent autophagy. In summary, our study demonstrates that SS-31 inhibits LPS-stimulated inflammation in HepG2 cells by upregulating ATG5-dependent autophagy.

中文翻译:

SS-31 通过增加 ATG5 并促进脂多糖刺激的 HepG2 细胞自噬来抑制炎症反应

SS-31 是一种靶向线粒体的短肽。最近的研究表明其具有保肝作用。在我们的研究中,我们研究了 SS-31 对 LPS 诱导的 HepG2 细胞自噬的影响。双荧光自噬检测系统的结果表明,SS-31促进自溶酶体和自噬体的形成,从而在一定程度上促进自噬流。此外,ELISA 和 qPCR 分析进一步证明 SS-31 通过 ATG5 依赖性自噬保护 HepG2 细胞免受 LPS 引发的炎症反应。总之,我们的研究表明 SS-31 通过上调 ATG5 依赖性自噬来抑制 HepG2 细胞中 LPS 刺激的炎症。
更新日期:2024-04-04
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