ZHANG Jia-fu, JIANG Hui, GAO Jia-rong, et al. Regulation of Ganle Granules on TGF-/Smad Signaling Pathways in Rats with Hepatic Fibrosis[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(6): 169-174.
ZHANG Jia-fu, JIANG Hui, GAO Jia-rong, et al. Regulation of Ganle Granules on TGF-/Smad Signaling Pathways in Rats with Hepatic Fibrosis[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(6): 169-174. DOI: 10.13422/j.cnki.syfjx.2017060169.
Objective: To study the regulation effect of Ganle granules(GLG) on transforming growth factor(TGF-β1)/Smad signaling pathways in rats with hepatic fibrosis
and to explore its possible mechanisms for prevention and treatment of hepatic fibrosis. Method: The SD rats were randomly divided into normal group
model group
GLG (1.5
3.0
6.0 g·kg-1) groups and colchicine (Col
0.1 mg·kg-1) group. The hepatic fibrosis rat models were induced by subcutaneous injection of CCl4(50%) twice each week for 12 weeks continuously. Then different doses of GLG (1.5
3.0
6.0 g·kg-1) and colchicines (0.1 g·kg-1) were administrated via gavage once a day for 6 weeks from week 7 after modeling. 8 h after the last administration
rats were sacrificed
and their liver samples were taken to observe the pathological and histological degree of liver fibrosis by HE and Masson. Moreover
the protein expression levels of CollagenⅠ
TGF-β1 and Smad2 or TβRⅠ in the liver tissues were determined by immunohistochemistry and Western blot. The mRNA expression levels of CollagenⅠ
Smad2
and TβRⅠin liver tissues were detected by the real-time fluorescent quantitative PCR. Result: As compared with the normal group
the pathological and histological degree of liver fibrosis
as well as protein and mRNA expression levels of Collagen I
TGF-β1
Smad2
and TβR I in model group were obviously increased in model group (P<0.01). As compared with model group
GLG middle and high doses not only obviously improved histopathological changes
but also effectively reduced the protein and/or mRNA expression levels of Collagen I
TGF-β1
Smad2
and TβR I (P<0.05
P<0.01). Conclusion: GLG has protective effect on liver fibrosis rats and its mechanism may be related to regulating the TGF-β1/Smad signaling pathways
inhibiting HSC activation
and reducing excessive extracellular matrix deposition.