- VernacularTitle: LRG1通过抑制p38/MAPK通路的活化缓解Aβ1-42诱导SH-SY5Y细胞损伤
- Author:
Tao KANG
1
;
Zheng HAN
1
;
Yanli XUE
1
Author Information
- Publication Type:Journal Article
- Keywords: Alzheimer’s disease;LRG1;Aβ1-42;Apoptosis;p38/MAPK
- From: Journal of Apoplexy and Nervous Diseases 2020;37(6):531-534
- CountryChina
- Language:Chinese
- Abstract: Objective To explore the role and mechanism of LRG1 in the cell model of Aβ1-42-induced Alzheimer’s disease (AD).Methods Aβ1-42 stimulated SH-SY5Y cells was used to build AD cell model in vitro.The cell counting kit-8 (CCK-8) was used to detect cell aviability.LRG1 transcriptional level was measured through real-time fluorescence quantitative PCR (RT-qPCR).The phosphorylation level of p38 and the protein levels of LRG1,Bcl-2 and Bax were detected by Western blot.Apoptosis rate was checked by flow CytoMetry.Results The results showed that treatment of Aβ1-42 in SH-SY5Y cells significantly reduced cell aviability and increased LRG1 protein level.LRG1 silencing promoted the cell aviability and inhibited apoptosis that induced by Aβ1-42.Silencing LRG1 reversed the changes of Bcl-2 and Bax protein levels which induced by Aβ1-42.Silencing LRG1 inhibited the phosphorylation of p38 that induced by Aβ1-42.In addition,U-46619 (p38 specific activator) reversed the protective effect of LRG1 silencing on Aβ1-42-treated SH-SY5Y cell damage.Conclusion These results suggest that LRG1 silencing alleviates cell injury that induced by Aβ1-42 through deactivating of the p38/MAPK signaling pathway.
- Full text:2024080122483337916LRG1 alleviates Aβ1-42-induced SH-SY5Y cell damage by inhibiting the activation of p38_MAPK pathway.pdf