Effects of Yinqi Sanhuang Jiedu Decoction （茵芪三黄解毒汤） on Liver Hardness and Epithelial Mesenchymal Transition in Hepatic Fibrosis Model Mice / 中医杂志

ABSTRACT

ObjectiveTo investigate the possible mechanism of compound Yinqi Sanhuang Jiedu Decoction （茵芪三黄解毒汤， YSJD） against the progression of hepatic fibrosis （HF）. MethodsThirty-eight C57BL/6J mice were randomly divided into blank group， model group， silybin group and low-， medium- and high-dose YSJD groups， with eight mice in the model group and six mice each in other groups. Except for the blank group， all mice were injected intraperitoneally with 10% carbon tetrachloride （CCl4） to establish a HF model， twice a week for 8 weeks. The drug intervention started one week after the first modeling； the low-， medium- and high-dose YSJD groups were given 8.325， 16.65 and 33.3 g/（kg·d） of YSJD suspension by gavage， respectively， while the silybin group was given 55 mg/（kg·d） of silybin suspension by gavage， and the blank group and the model group were given 0.2 ml normal saline by gavage， all for 8 weeks. The liver hardness of living mice was observed using a small animal ultrasound detector， and grey-scale ultrasound was recorded. The liver tissue was observed by Sirius scarlet staining， and the proportion of collagen fiber deposition was calculated. Liver function indicators including alanine aminotransferase （ALT） and aspartate aminotransferase （AST）， and serum laminin （LN）， hyaluronic acid （HA）， pre-collagen type III （PCIII） and collagen type IV （CIV） were also detected. The protein expression of transforming growth factor β1 （TGF-β1）， Vimentin， E-cadherin， α smooth muscle actin （α-SMA） in liver tissue were detected. ResultsCompared to the blank group， the model group showed increased gray value， collagen deposition，serum ALT， AST， HA， LN and PCIII levels， decreased expression of E-cadherin， and increased expression of N-cadherin，α-SMA，Vimentin and TGF-β1 in liver tissues （P＜0.05）. Compared to the model group， the ultrasonic gray value and the proportion of collagen fiber deposition in liver of silybin group and YSJD medium- and high-dose groups decreased， and the serum ALT， AST， LN， HA and PCⅢ levels decreased. Compared to the model group， the expression of E-cadherin in liver tissues of silybin group and all three YSJD groups increased， while the expressions of N-cadherin， Vimentin， TGF-β1 and α-SMA decreased （P＜0.05）， and among them， most improvements were seen in the medium-dose YSJD group （P＜0.05）. ConclusionThe effect of YSJD on significantly reducing the extent of HF in mice caused by CCl4 may be related to its ability to regulate liver hardness and inhibit the occurrence of epithelial mesenchymal transition in mice.