Study on mechanism of salidroside against liver fibrosis by regulating CXCL16.
10.19540/j.cnki.cjcmm.20201224.401
- Author:
Qian-Nan YE
1
;
Chang-Qing ZHAO
2
;
Jian PING
3
;
Lie-Ming XU
4
Author Information
1. Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine Shanghai 201203, China Institute of Hepatology, Shanghai University of Traditional Chinese Medicine Shanghai 201203, China.
2. Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine Shanghai 201203, China Institute of Hepatology, Shanghai University of Traditional Chinese Medicine Shanghai 201203, China Key Laboratory of Liver and Kidney Diseases, Ministry of Education Shanghai 201203, China.
3. Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine Shanghai 201203, China Key Laboratory of Liver and Kidney Diseases, Ministry of Education Shanghai 201203, China.
4. Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine Shanghai 201203, China Institute of Hepatology, Shanghai University of Traditional Chinese Medicine Shanghai 201203, China Key Laboratory of Liver and Kidney Diseases, Ministry of Education Shanghai 201203, China Shanghai Key Clinical Laboratory of Traditional Chinese Medicine Shanghai 201203, China.
- Publication Type:Journal Article
- Keywords:
CXCL16;
hepatic stellate cells;
liver fibrosis;
salidroside
- MeSH:
Animals;
Carbon Tetrachloride;
Chemokine CXCL16;
Glucosides;
Hepatic Stellate Cells;
Liver/pathology*;
Liver Cirrhosis/genetics*;
Male;
Mice;
Phenols
- From:
China Journal of Chinese Materia Medica
2021;46(11):2865-2870
- CountryChina
- Language:Chinese
-
Abstract:
In order to investigate the effect of salidroside on inhibiting liver fibrosis and its relationship with CXC chemokine ligand 16(CXCL16) in vivo and in vitro, totally 45 C57 BL/6 J male mice were randomly divided into normal group, model group and salidroside group, with 15 mice in each group. The mice in model group and salidroside group were injected intraperitoneally with 15% carbontetrachloride(CCl_4) olive oil solution to establish liver fibrosis model, and the mice in normal group were injected intraperitoneally with the same dose of olive oil. Salidroside group was given with 100 mg·kg~(-1 )salidroside by gavage, while the normal group and model group received the same amount of double distilled water by gavage. All mice were sacrificed after 5 weeks of intragastric administration. The pathological changes of mouse liver were observed by hematoxylin-eosin(HE) staining, and the degree of liver fibrosis was observed by sirius red staining. The protein expressions of collagen Ⅰ(ColⅠ), α-smooth muscle actin(α-SMA), fibronectin(FN), CXCL16, phosphorylated Akt(p-Akt), Akt in liver tissues were detected by Western blot. Hepatic stellate cell line JS 1 was cultured in vitro and divided into control group, model group(100 μg·L~(-1) CXCL16) and salidroside group(100 μg·L~(-1) CXCL16+1×10~(-5) mol·L~(-1) salidroside). Cell migration was detected by cell scratch, the mRNA expressions of ColⅠ and α-SMA were detected by RT-PCR, and the protein expressions of p-Akt and Akt were detected by Western blot. As compared with the normal group, the protein expressions of ColⅠ, α-SMA, FN, CXCL16, and p-Akt in the model group were significantly increased, and salidroside could reduce the expression of these indicators(P<0.05 or P<0.01). In vitro, CXCL16 could promote the migration of JS 1, increase the mRNA expressions of ColⅠ and α-SMA in JS 1, and enhance Akt phosphorylation in JS 1(P<0.05 or P<0.01). As compared with the model group, salidroside could inhibit the migration of JS 1 induced by CXCL16(P<0.05), and reduce the high expression of ColⅠ and α-SMA mRNA and the phosphorylation of Akt in JS 1 induced by CXCL16(P<0.05). In conclusion, salidroside might attenuate CCl_4-induced liver fibrosis in mice by inhibiting the migration, activation and Akt phosphorylation of hepatic stellate cells induced by CXCL16.
