Study on mechanism of curcumol against liver fibrosis based on autophagy and apoptosis of hepatic stellate cells.
10.19540/j.cnki.cjcmm.20210930.401
- Author:
Yang ZHENG
1
;
Can-Li XU
1
;
Neng-Yuan LU
1
;
Fei-Fei QIU
1
;
Ying-Jie ZHAO
1
;
Yu-Xian CHANG
1
;
Jia-Hui WANG
1
;
Tie-Jian ZHAO
1
;
Xian-Ling YUAN
2
Author Information
1. Department of Medicine, Faculty of Chinese Medicine Science, Guangxi University of Chinese Medicine Nanning 530222, China.
2. Teaching Experiment Training Center, Guangxi University of Chinese Medicine Nanning 530222, China.
- Publication Type:Journal Article
- Keywords:
apoptosis;
autophagy;
curcumol;
hepatic stellate cells;
liver fibrosis
- MeSH:
Actins/metabolism*;
Apoptosis;
Autophagy;
Hepatic Stellate Cells;
Humans;
Liver/metabolism*;
Liver Cirrhosis/metabolism*;
Sesquiterpenes;
Transforming Growth Factor beta1/metabolism*
- From:
China Journal of Chinese Materia Medica
2022;47(3):730-736
- CountryChina
- Language:Chinese
-
Abstract:
The present study clarified the molecular mechanism of curcumol against liver fibrosis based on its effects on the autopha-gy and apoptosis of hepatic stellate cells. The hepatic stellate cells were divided into a blank control group, a transforming growth factor-β1(TGF-β1)(10 ng·mL~(-1)) group, and low-(12.5 mg·L~(-1)), medium-(25 mg·L~(-1)), and high-dose(50 mg·L~(-1)) curcumol groups. The effect of curcumol on the viability of hepatic stellate cells induced by TGF-β1 was detected by the MTT assay kit. The apo-ptosis in each group was determined by flow cytometry. Real-time fluorescence-based quantitative PCR(RT-PCR) was employed for the detection of mRNA expression of α-smooth muscle actin(α-SMA), type Ⅰ collagen(collagen Ⅰ), and type Ⅲ collagen(collagen Ⅲ). Western blot was used to detect the protein expression of p62, microtubule-associated protein 1 light chain 3(LC3), beclin1, B cell lymphoma 2(Bcl-2), and Bcl-2-associated X protein(Bax). Transmission electron microscopy(TEM) was used to observe cell morphology and autophagosome formation in each group. The autophagic flux was observed after cell infection with adenovirus under double fluorescence labeling. The cell viability assay revealed that compared with the TGF-β1 group, the curcumol groups showed significantly decreased cell viability. The apoptosis assay showed that the apoptosis rates of the curcumol groups were significantly higher than that of the TGF-β1 group. RT-PCR indicated that the mRNA expression of α-SMA, collagenⅠ, and collagen Ⅲ in the curcumol groups was significantly lower than that of the TGF-β1 group. Western blot showed that the expression of p62, LC3, beclin1, Bcl-2, and Bax in the curcumol groups was significantly different from that in the TGF-β1 group. As demonstrated by TEM, compared with the TGF-β1 group, the curcumol groups showed significantly increased autophagosomes. The detection of autophagic flow by the adenovirus under double fluorescence labeling showed that autolysosomes in the curcumol groups were significantly increased compared with those in the TGF-β1 group. Curcumol can induce the autophagy and apoptosis of hepatic stellate cells, which may be one of its anti-liver fibrosis mechanisms.
