San-Cao Granule () Ameliorates Hepatic Fibrosis through High Mobility Group Box-1 Protein/Smad Signaling Pathway.
- Author:
Shi-Zhang WEI
1
;
Sheng-Qiang LUO
2
;
Jian WANG
1
;
Jia-Bo WANG
3
;
Rui-Sheng LI
4
;
Xiao-Mei ZHANG
1
;
Yan-Lei GUO
5
;
Chang CHEN
1
;
Xiao MA
1
;
Zhe CHEN
1
;
Hong-Hong LIU
2
;
Zhi-Rui YANG
1
;
Jian-Yu LI
2
;
Rui-Lin WANG
2
;
Ya-Ming ZHANG
3
;
Hui-Yin YANG
2
;
Xiao-He XIAO
3
;
Yan-Ling ZHAO
6
,
7
Author Information
- Publication Type:Journal Article
- Keywords: San-Cao Granule; high mobility group box-1 protein; liver fibrosis; toll-like receptor 4/nuclear factor-kappa B; transforming growth factor β1/mothers against decapentaplegic homolog
- MeSH: Animals; Disease Models, Animal; Drugs, Chinese Herbal; therapeutic use; HMGB1 Protein; metabolism; Liver; drug effects; metabolism; pathology; Liver Cirrhosis; drug therapy; metabolism; pathology; Male; Rats; Rats, Sprague-Dawley; Signal Transduction; drug effects; Smad Proteins; metabolism
- From: Chinese journal of integrative medicine 2018;24(7):502-511
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the possible mechanism of San-Cao Granule (SCG, ) mediating antiliver fibrosis.
METHODSA total of 60 male Sprague-Dawley rats were randomly divided into the normal control group, porcine serum-treated group, ursodesoxycholic acid (UDCA, 60 mg/kg), SCG (3.6 g/kg) group, SCG (1.8 g/kg) group and SCG (0.9 g/kg) group, with 10 rats in each group. Liver fibrosis was induced with porcine serum by intraperitoneal injection for 8 weeks, except for the normal control group. Then, the rats in the three SCG-treated groups and UDCA group were administered SCG and UDCA respectively for 4 weeks. The serum levels of alanine transaminase (ALT), aspartate transaminase (AST), albumin (ALB), total bilirubin (TBIL), hyaluronic acid (HA), laminin (LN), and type IV collagen (IVC) were examined using commercial kits and hepatic histopathology was examined with hematoxylin and eosin and Masson staining. Moreover, the protein expression levels of high mobility group box-1 protein (HMGB1), transforming growth factor β1 (TGF-β1), phosphorylated mothers against decapentaplegic homolog 3 (p-Smad3), Smad7, toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), nuclear factor-kappa B (NF-κB) and α-smooth muscle actin (α-SMA) were determined by western blot, immunohistochemistry and real time quantitative-reverse transcription polymerase.
RESULTSBoth SCG (3.6 and 1.8 g/kg) and UDCA significantly ameliorated the liver fibrosis induced by porcine serum as indicated by retarding the serum levels increasing of ALT, AST, TBIL, HA, LN and IVC and preventing the serum level reducing of ALB compared with the model group (all P<0.01). Meanwhile, the collagen deposition was attenuated by SCG and UDCA treatment. Furthermore, SCG markedly reduced the expressions of HMGB1, TGF-β1, p-Smad3, TLR4, MyD88, NF-κB and α-SMA, and enhanced the expression of the Smad7 compared with the model group (all P<0.01).
CONCLUSIONSCG ameliorates hepatic fibrosis possibly through inhibiting HMGB1, TLR4/NF-κB and TGF-β1/Smad signaling pathway.
