Effect of emodin on apoptosis and oxidative damage of PC12 cells induced by hypoxia/reoxygenation based on NGF/TrkA pathway
10.3969/j.issn.1000-484X.2025.03.010
- VernacularTitle:基于NGF/TrkA通路探究大黄素对缺氧/复氧诱导的PC12细胞凋亡及氧化损伤的影响
- Author:
Changying LYU
1
;
Junli BIAN
;
Wei LI
Author Information
1. 济南市中西医结合医院脑病三科,济南 271100
- Publication Type:Journal Article
- Keywords:
Hypoxia/reoxygenation;
PC12;
Apoptosis;
Oxidative damage;
Nerve growth factor/tropomyosin receptor kinase A
- From:
Chinese Journal of Immunology
2025;41(3):566-570
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To analyze the effect of emodin on apoptosis and oxidative damage of PC12 cells induced by hypoxia/re-oxygenation and its corresponding mechanism.Methods:PC12 cells were cultured in vitro and their neural differentiation was induced.Cells were divided into control group,model group,low concentration emodin group(30 mmol/L),high concentration emodin group(90 mmol/L)and high concentration emodin+GW441756(90 mmol/L+6.3 μmol/L)group,excepted for control group,other groups were treated with hypoxia and reoxygenation,and viability of PC12 cells was determined by CCK-8 method;levels of LDH release,SOD,MDA,IL-1β and TNF-α were measured by kits;PC12 cell apoptosis was detected by flow cytometry,expressions of nerve growth factor(NGF)/tropomyosin receptor kinase A(TrkA)pathway proteins in PC12 cells were determined by Western blot.Results:Compared with control group,PC12 cell activity,SOD level,NGF,and p-TrkA/TrkA in model group were decreased(P<0.05),while LDH release,apoptosis rate,MDA,IL-1β and TNF-α levels were increased(P<0.05);compared with model group,PC12 cell activity,SOD level,NGF,and p-TrkA/TrkA in low concentration emodin group and high concentration emodin group were increased(P<0.05),while LDH release,apoptosis rate,MDA,IL-1β and TNF-α levels were decreased(P<0.05);compared with high concen-tration emodin group,PC12 cell activity,SOD level,NGF,and p-TrkA/TrkA in high concentration emodin+GW441756 group were decreased(P<0.05),while LDH release,apoptosis rate,MDA,IL-1β and TNF-α levels were increased(P<0.05).Conclusion:Emodin can inhibit oxidative stress and inflammatory damage of PC12 cells induced by hypoxia/reoxygenation,and inhibit apoptosis by activating NGF/TrkA pathway.
