Effect of compound rhodiola sachalinensis A Bor on CCI4-induced liver fibrosis in rats and its probable molecular mechanisms
AIM: To explore the anti-fibrotic effect of a traditional Chinese medicine, compound rhodiola sachalinensis A Bor on CCl4-induced liver fibrosis in rats and its probable molecular mechanisms. METHODS: Ninety healthy male SD rats were randomly divided into three groups: normal group (n=-10), treatmen...
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Veröffentlicht in: | World journal of gastroenterology : WJG 2003, Vol.9 (7), p.1559-1562 |
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Zusammenfassung: | AIM: To explore the anti-fibrotic effect of a traditional Chinese medicine, compound rhodiola sachalinensis A Bor on CCl4-induced liver fibrosis in rats and its probable molecular mechanisms. METHODS: Ninety healthy male SD rats were randomly divided into three groups: normal group (n=-10), treatment group of compound rhodiola sachalinensis A Bor (n=-40) and CCl4-induced model group (n=40). The liver fibrosis was induced by CCl4 subcutaneous injection. Treatment group was administered with compound rhodiola sachalinensis A Bor (0.5 g/kg) once a day at the same time. Then the activities of several serum fibrosis-associated enzymes: alanine aminotransferase (ALT), aspartate aminotransferase (AST), N-acetyl-beta-D-glucosaminidase (β-NAG) and the levels ofserum procollagen Ⅲ (PCⅢ), collagen Ⅳ (CⅣ), hyaluronic acid (HA) were assayed. The histooathol(mical chanaes were observed with HE, VG and Masson stain. The expression of TGF-β1 mRNA,αl (I) mRNA and Na+/Ca2+ exchanger (NCX ) mRNA was detected by reverse transcription polymerase chain reaction (RT-PCR) in situ.RESULTS: Compound rhodiola sachalinensis A Bor significantly reduced serum activities of ALT, AST, β-NAG and decreased the levels of PCⅢ, CⅣ, HA, improved the liver histopathological changes, inhibited the expression of TGF-β1 mRNA, α(1) mRNA and Na+/Ca2+ exchanger mRNA in rats. CONCLUSION: Compound rhodiola sachalinensis A Bor can intervene in CCI4-induced liver fibrosis in rats, in which potential mechanisms may be decreasing the production of TGF-β1, reducing the production of collagen, preventing the activation of hepatic stellate cell (HSC) and inhibiting theexpression of TGF-β1 mRNA, αl(I) mRNA and Na+/Ca2+ exchanger mRNA. |
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ISSN: | 1007-9327 2219-2840 |