Involvement of mitochondrial apoptotic pathway and MAPKs/NF-κ B inflammatory pathway in the neuroprotective effect of atractylenolide III in corticosterone-induced PC12 cells.
10.1016/S1875-5364(19)30030-5
- Author:
Wen-Xia GONG
1
;
Yu-Zhi ZHOU
2
;
Xue-Mei QIN
3
;
Guan-Hua DU
4
Author Information
1. Modern Research Center for Traditional Chinese Medicine, Shanxi University, Taiyuan 030006, China.
2. Modern Research Center for Traditional Chinese Medicine, Shanxi University, Taiyuan 030006, China. Electronic address: zhouyuzhi@sxu.edu.cn.
3. Modern Research Center for Traditional Chinese Medicine, Shanxi University, Taiyuan 030006, China. Electronic address: qinxm@sxu.edu.cn.
4. Modern Research Center for Traditional Chinese Medicine, Shanxi University, Taiyuan 030006, China; Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.
- Publication Type:Journal Article
- Keywords:
Apoptosis;
Atractylenolide III;
Corticosterone;
Depression;
MAPKs;
NF-ΚB
- MeSH:
Animals;
Apoptosis;
drug effects;
Calcium;
metabolism;
Cell Survival;
drug effects;
Corticosterone;
toxicity;
Inflammation Mediators;
metabolism;
L-Lactate Dehydrogenase;
metabolism;
Lactones;
pharmacology;
Mitochondria;
drug effects;
metabolism;
Mitogen-Activated Protein Kinases;
metabolism;
NF-kappa B;
metabolism;
Neuroprotective Agents;
pharmacology;
PC12 Cells;
Phosphorylation;
drug effects;
Rats;
Sesquiterpenes;
pharmacology;
Signal Transduction;
drug effects
- From:
Chinese Journal of Natural Medicines (English Ed.)
2019;17(4):264-274
- CountryChina
- Language:English
-
Abstract:
Atractylenolide III (ATL-III), a sesquiterpene compound isolated from Rhizoma Atractylodis Macrocephalae, has revealed a number of pharmacological properties including anti-inflammatory, anti-cancer activity, and neuroprotective effect. This study aimed to evaluate the cytoprotective efficiency and potential mechanisms of ATL-III on corticosterone injured rat phaeochromocytoma (PC12) cells. Our results demonstrate that ATL-III increases cell viability and reduces the release of lactate dehydrogenase (LDH). The results suggest that ATL-III protects PC12 cells from corticosterone-induced injury by inhibiting the intracellular Ca overloading, inhibiting the mitochondrial apoptotic pathway and modulating the MAPK/NF-ΚB inflammatory pathways. These findings provide a novel insight into the molecular mechanism by which ATL-III protected the PC12 cells against corticosterone-induced injury for the first time. Our results provide the evidence that ATL-III may serve as a therapeutic agent in the treatment of depression.
