Molecular Mechanism Of ERS Induced By Lipid Accumulation In Human Mesangial Cells (HMCs) Injury

Aim: To investigate the molecular mechanism of ERS induced by lipidaccumulation in human mesangial cells (HMCs) injury.Methods:HMCs were cultured and divided into normal group,inflammatory group(IL-β),high lipid group(LDL),combination treatmentgroup (LDL plus IL-1β),and4-PBA intervention group(4-PBA plus LDLplus IL-1β). Oil Red O staining was used for the observation of lipid dropletaccumulation in the cells,and Real-time PCR was used for the mRNA levelsof GRP78,PERK and α-SMA,Western blotting was used for the expressionof GRP78,PERK and NF-κB p65,ELISA was used for the secretion of IL-6in the culture supernatant.Results:1.Compared with the normal group, the intracellular lipidaccumulationm,the level of GRP78,PERK,the NF-κB p65,the secretion ofIL-6,α-SMA mRNA in the IL-1βgroup,LDL group,and combinationtreatment group was overt increased((P＜0.05,respectively);2. Comparedwith the IL-1β group,LDL group, the lipid accumulationm, the mRNA andprotein expression of those above genes in the combination treatmentgroup were increased remarkably (P＜0.05, respectively);3.when intervened by4-PBA,those genes were dramatically down-regulated(P＜0.05respectively s the combination treatment group).Conclusion: Inflammatory can exacerbrate lipid-induced ER-stress inHMCs,cause phenotype transformation,and then futher aggravate localinflammation response of kindey,while interfering ERS can play a better rolein renal protection.