Effects and mechanisms of SNP-9 on Aβ25-35-induced damage in bEnd.3 cells
10.11665/j.issn.1000-5048.20220311
- VernacularTitle:SNP-9对Aβ25-35导致bEnd.3细胞损伤的作用及其机制
- Author:
Yue MENG
1
;
Siyuan YAO
;
Xiangdong GAO
;
Song CHEN
Author Information
1. 中国药科大学生命科学与技术学院
- Publication Type:Journal Article
- Keywords:
SNP-9;
Alzheimer′s disease;
blood-brain barrier;
bEnd.3;
Aβ25-35;
NF-κB
- From:
Journal of China Pharmaceutical University
2022;53(3):333-339
- CountryChina
- Language:Chinese
-
Abstract:
In order to investigate the effects of neuroprotective peptide SNP-9 which is derived from silk fibroin hydrolysate on the injury of the blood-brain barrier in Alzheimer′s disease (AD), Aβ25-35 was used to damage brain microvascular endothelial cells bEnd.3 to establish AD injury model and drug intervention was performed.MTT assay was used to detect the effects of SNP-9 and Aβ25-35 on cell viability.RT-qPCR was used to determine the effects of SNP-9 and Aβ25-35 on the mRNA levels of tight junctions (TJs)-related ZO-1, occludin and claudin-5.Western blot was used to detect the effects of SNP-9 and Aβ25-35 on the protein levels of TNF-α, phosphorylated NF-κB, NF-κB, IκBα and RAGE.The results showed that SNP-9 reduced bEnd.3 cell damage induced by Aβ25-35, and improved the abnormal mRNA levels of ZO-1, occludin and claudin-5 in model cells.It alleviated the abnormal protein levels of TNF-α, phosphorylated NF-κB, IκBα and RAGE induced by Aβ25-35. These results suggest that SNP-9 may regulate the levels of TNF-α in model cells by influencing RAGE/NF-κB pathway, and then ameliorate TJs-related abnormalities and alleviate bEnd.3 cell injury induced by Aβ25-35.
