| Objective: Lipotoxicity is related to the progression of many sicknesses.Long-term exposure to high fat levels could easily lead to a lot of abnormal signal activation,resulting in inflammation.In this study,we studied the NAFLD rats fed with HFD and the PA induced liver cells to investigate whether the mTORC1 pathway associated with inflammation.Furthermore,we studied whether the GLP-1 analogue(liraglutide)protects the body from lipotoxicity induced cellular and animal inflammatory damage and its molecular mechanisms.Methods: Rats were fed with HFD to establish NAFLD model and were treated with liraglutide.They were divided into three groups according to different treatments.The body weight,liver index,food intake and GIR of the rats were recorded.The histological morphology of liver sections of stained rats were observed under microscope and assess related enzymes of liver function in serum.After extracting animal liver and cell proteins,Western blot was used to evaluate the changes of related molecules of mTORC1 pathway and NLRP3.Hep G2 cells were treated with PA and liraglutide to detect intracellular TG content and inflammatory factors in supernatant.Results: Our results showed that lipotoxicity could induce significant inflammatory responses in cells and animals by activating the mTORC1 pathway,while PA-treated Hep G2 cells treated with rapamycin could improve the inflammatory responses caused by PA to a certain extent.In addition,we found that liraglutide can ameliorate inflammation caused by lipotoxicity through activating mTORC1 pathway.Conclusion: 1.Lipid toxicity can induce liver inflammation.2.liraglutide can improve lipotoxicity-induced inflammation.3.liradlutide may regulate mTORC1 signaling pathway to treat lipotoxicity-induced inflammation. |
