Metformin alleviates inflammation through suppressing FASNdependent palmitoylation of Akt
Wenfang Xiong1,4 , Kuo-Yang Sun2,4 , Yan Zhu1 , Xiaoqi Zhang1, Yi-Hua Zhou3 and Xiaoping Zou 1
Abstract: Metformin, traditionally regarded as a hypoglycemic drug, has been studied in other various fields including inflammation. The specific mechanism of metformin’s effect on immune cells remains unclear. Herein, it is verified that LPS-induced macrophages are characterized by enhanced endogenous fatty acid synthesis and the inhibition of fatty acid synthase (FASN) downregulates proinflammatory responses. We further show that metformin could suppress such elevation of FASN as well as proinflammatory activation in macrophages. In vivo, metformin treatment ameliorates dextran sulfate sodium (DSS)-induced colitis through impairing proinflammatory activation of colonic lamina propria mononuclear cells (LPMCs). The reduction of FASN by metformin hinders Akt palmitoylation, which further disturbs Akt membrane attachment and its phosphorylation. Metformin-mediated suppression of FASN/Akt pathway and its downstream MAPK signaling contributes to its anti-inflammatory role in macrophages. From the perspective of immunometabolism, our work points towards metformin utilization as an effective and potential intervention against macrophages-involved inflammatory diseases.
详情请见：https://doi.org/10.1038/s41419-021-04235-0
在该研究中圣尔生物通用型ECL发光液用于Western blotting实验
Western blotting
Specific signaling was generated using chemiluminescent substrate (Share-Bio, sb-wb012) and recorded with a CCD camera
