CAO Wen, LIAO Ming, ZHOU Yan, et al. Therapeutic Effects and Mechanisms of Combined Therapy of Taurine, Epigallocatechin Gallate, and Genistein on Liver Fibrosis in Rats[J]. Chinese journal of experimental traditional medical formulae, 2015, 21(4): 107-111.
DOI:
CAO Wen, LIAO Ming, ZHOU Yan, et al. Therapeutic Effects and Mechanisms of Combined Therapy of Taurine, Epigallocatechin Gallate, and Genistein on Liver Fibrosis in Rats[J]. Chinese journal of experimental traditional medical formulae, 2015, 21(4): 107-111. DOI: 10.13422/j.cnki.syfjx.2015040107.
Therapeutic Effects and Mechanisms of Combined Therapy of Taurine, Epigallocatechin Gallate, and Genistein on Liver Fibrosis in Rats
n=12) and high (taurine 200 mg · kg-1+EGCG 30 mg · kg-1+genistein 20 mg · kg-1
n=12) dose group. The rats except normal group were induced by intragastric administration (ig) of 50%CCl4 for 14 weeks
and the normal group was given peanut oil. Treatment was started at the 9th week for 6 weeks. Rats were sacrificed after the last administration
and the serum and liver tissue were taken quickly. The levels of alanine aminotransferase(ALT)
aspartate aminotransferase(AST)
transforming growth factor β1(TGF-β1) and collagen I in serum and total antioxidamt capacity(T-AOC)
superoxide dismutase(SOD) and glutathione peroxidase(GSH-Px) activities in liver were measured
and HE staining was performed to evaluate histopathologic changes. Result: Compared with normal group
levels of ALT
AST
TGF-β1 and collagen I increased and liver T-AOC
SOD and GSH-Px activities decreased significantly in the model group (P<0.05). Compared with the model group
levels of ALT
AST
TGF-β1 and collagen I decreased significantly in combined therapy of middle and high dose group
and liver T-AOC
SOD and GSH-Px activities increased significantly in combined therapy of high dose group (P<0.05). Conclusion: Combined therapy has certain curative effect on CCl4-induced liver fibrosis in rats. Its mechanism may involve scavenging free radical
alleviating the lipid peroxidation
inhibiting the expression of TGF-β1 and reducing the synthesis of extracellular matrix.
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