Rhaponticum uniflorum inhibits H2O2-induced apoptosis of liver cells via JNK and NF-κB pathways.
10.19540/j.cnki.cjcmm.20170121.013
- Author:
Xin HE
1
;
Chun-Yan LIU
1
;
Ji-Feng YIN
2
;
Ai-Hua JIN
2
;
Xue-Zhe YIN
2
;
Ji-Shu QUAN
1
Author Information
1. Medical College, Yanbian University, Yanji 133002, China.
2. Affiliated Hospital of Yanbian University, Yanji 133000, China.
- Publication Type:Journal Article
- Keywords:
H2O2;
HepG2;
Rhaponticum unifloru;
apoptosis;
oxidative stress
- From:
China Journal of Chinese Materia Medica
2017;42(6):1189-1193
- CountryChina
- Language:Chinese
-
Abstract:
To study the inhibitory effect of Rhaponticum uniflorum on apoptosis induced by H2O2 in HepG2 cells. Human HepG2 cells injury models were established by H2O2, then cell survival rate was assayed by MTT method; levels of LDH, ALT, and AST were detected by chemical colorimetric method;SOD activity was detected by xanthine oxidase method; GSH content was detected by dithio-bis-nitrobenzoic acid(DTNB); MDA level was detected by thiobarbituric acid (TBA) method;and the relative activities of Caspase-3, 8 and 9 were measured by Colorimetry. The expression levels of Cleaved Caspase-3(Casp-3), cytochrome(Cyto c), NF-κB, ERK, JNK, p38 MAPK, as well as the phospharylated proteins were determined with Western blotting method. The results showed that R. unifloru had no significant effect on cell viabilities of HepG2 cells at the concentrations of 25-400 mg•L⁻¹. However, H2O2decreased the cell viabilities, increased the cellular oxidative stress, and up-regulated the protein expressions of Casp-3, cytoplasmic Cyto c, p-JNK and nuclear NF-κB. As compared with the model group,R. unifloru could increase the cell viability, reduce LDH, ALT and AST leakage, reduce the MDA formation, increase the SOD and GSH levels,reduce the relative activities of Caspase-3, 8 and 9, down-regulated the protein expressions of Casp-3 and cytoplasmic Cyto c, and down-regulate the p-JNK and nuclear NF-κB levels.The results indicated that R. unifloru had the inhibitory effect on apoptosis induced by H2O2in HepG2 cells, and the mechanism maybe associated with inhibiting JNK activation and NF-κB nuclear translocation.
