Protective effect and mechanism of active peptide GRGDS on PC12 cells damage by oxygen-glucose deprivation
10.12206/j.issn.1006-0111.202007053
- VernacularTitle:活性多肽GRGDS对氧糖剥夺诱导PC12细胞损伤的保护作用及其机制研究
- Author:
Cheng ZHANG
1
;
Jianping MA
1
;
Yuhua SHEN
1
;
Wenjun ZHU
1
;
Helong LIU
1
;
Yan QIU
1
Author Information
1. Department of Pharmacy, Pudong New Area People's Hospital Affiliated to Shanghai University of Medicine & Health Sciences, Shanghai 201200, China.
- Keywords:
active peptide;
GRGDS;
oxygen glucose deprivation;
PC12 cells;
apoptosis
- From:
Journal of Pharmaceutical Practice
2021;39(4):317-321
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the protective effect of active peptide GRGDS on rat nerve cells (PC12 cells) in oxygen glucose deprivation (OGD) injury model and explore its mechanism of action. Methods PC12 cells were divided into control group, ODG group, and active peptide GRGDS treatment group. The injury model was established by simulating in vitro cerebral ischemia by oxygen and sugar deprivation. MTT and flow cytometry were used to detect apoptosis after oxygen-glucose deprivation. ELISA method was used to detect the changes of inflammatory factors TNF-α and IL-1β in PC12 cell supernatant after oxygen-glucose deprivation. Western blot was used to detect the expression of apoptosis pathway-related proteins. Results The results of MTT and flow cytometry showed that the active peptide GRGDS significantly reduced the apoptosis of PC12 cells after oxygen glucose deprivation (P<0.05). ELISA test results showed that the active peptide GRGDS significantly reduced the content of TNF-α and IL-1β in the supernatant of PC12 cells after oxygen-glucose deprivation. (P<0.05). Western blot results showed that the active peptide GRGDS significantly reduced the expression levels of p-JNK, Bax, and cleaved caspase 3 in PC12 cells mediated by oxygen-glucose deprivation injury (P <0.01). Conclusion The active peptide GRGDS has protective effect on PC12 cells damaged by oxygen and glucose deprivation. The mechanism may be related to anti-apoptotic and anti-inflammatory effects.
