山楂总黄酮对四氯化碳致大鼠肝纤维化的保护作用及其机制研究

目的:观察山楂总黄酮对四氯化碳(CCl4)致大鼠肝纤维化的保护作用,并初步探讨其作用机制。方法:用CCl4复制大鼠中毒性肝纤维化模型,观察山楂总黄酮对大鼠血清中丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、白蛋白(Alb),肝组织病理学及超氧化物歧化酶(SOD)、丙二醛(MDA)、羟脯氨酸(Hyp)的影响;免疫组化方法测定肝组织α-平滑肌肌动蛋白(α-SMA)和转化生长因子β1(TGF-β1)的表达。结果:与模型组相比,山楂总黄酮给药组血清学指标ALT、AST浓度明显降低,Alb浓度升高,肝组织内SOD浓度升高,MDA、Hyp浓度降低,且肝组织中α-SMA和TGF-β1的表达显著降低,差异均有统计学意义(P<0.05)。结论:山楂总黄酮对CCl4致大鼠肝纤维有较好的保护作用,其机制可能与减少自由基生成、减轻脂质过氧化及抑制α-SMA和TGF-β1的表达有关。

Preventive effect and mechanism of hawthorn flavonoids on rat hepatic fibrosis induced by carbon tetrachloride

Objective： To investigate the protective effect and mechanism of hawthorn flavonoids on CCl4-induced hepatic fibrosis in rats. Methods： Hepatic fibrosis models were induced by subcutaneous injection of CCl4in rats. The level of alanine aminotransferase（ ALT）,aspartate aminotransferase（ AST）,albumi（ Alb） in serum,and superoxide dismutase（ SOD）,malondialdehyde（ MDA）,hydroxyproline（ Hyp） in hepatic tissue was detected to analyze the effect of hawthorn flavonoids. The expression of α-smooth muscle actin（ α-SMA） and transforming growth factor β1（ TGF-β1） in liver tissue were detected by immunohistochemistry. Results： Compared with model group,Hawthorn flavonoids treatment groups had a lower level of ALT,AST in serum and Hyp,MDA in liver tissue,while the level of Alb in serum and SOD in liver tissue was increased. The expression of α-SMA and TGF-β1 was inhibited significantly. The difference was statistically significant（ P 0. 05）. Conclusion： Hawthorn flavonoids could inhibite experimental hepatic fibrosis formation. The possible mechanisms were hawthorn flavonoids reducing the generation of free radicals,decreasing lipid peroxidation and inhibiting the expression of α-SMA and TGF-β1.