The protective effects of salvianolic acid B, ginsenoside Rgl and notoginsenoside R1 on oxygen-glucose deprivation/reoxygenation and reoxygenation of astrocytes
- Author:
Juan YANG
1
;
Yu-Shuang CAO
1
;
Yao XU
1
;
Xin-Yuan DU
1
;
Tong ZHANG
1
;
Li-Chen GUO
1
;
Qing YUAN
1
;
Li-Juan CHAL
1
;
Li-Min HU
1
Author Information
- Publication Type:Journal Article
- Keywords: astrocytes; ginsenoside Kgl; ne urotrophic factor; notoginsenoside HI; OGD/K; oxidative damage; salvianolate acid B
- From: Chinese Pharmacological Bulletin 2022;38(10):1466-1472
- CountryChina
- Language:Chinese
- Abstract: eration-toxicity test kit was used to detect the cell viability of astrocytes, and flow cytometry to detect mitochondrial membrane potential, KOS release and intracellular calcium concentration.KT-PCK was employed to detect the niHNA expression of BDNF, NGF, KtFIcx in astrocytes.Western blot was used to detect the phosphorylation of PI3K, ART and STA'13 protein in astrocytes.Results OGD/K significantly decreased cell viability.HOS release and intracellular calcium ion concentration of astrocytes, mitochondrial membrane potential and p-STAT3 , p-PI3K, p-AKT ex¬pression decreased in OGD/R group.Sal 15, Rgl and HI significantly increased the viability of damaged cells, and regulated KOS release, calcium ion concen¬tration and mitochondrial membrane potential to varying degrees.Sal B and Rgl increased the expression of p- STA'13 and p-AKT.Hie expression of BDNF and NGF niRNA in OGD/R group significantly decreased, and Sal B, Hgl and HI could significantly increase the ex¬pression of BDNF niHNA in damaged cells.Hgl could increase NGF niRNA expression.Sal B increased the expression of IGFla niRNA.Conclusions Sal B, Kgl, and HI reduce the oxidative stress response of astrocytes after OGD/R injury by regulating the PI3K/ ART and STA'13 signaling pathway, reduce intracellu¬lar calcium overload, and play a protective role in as-trocytes, increase the release of astrocyte neurotrophic factor, which may further play a protective role in neu¬rons.
