二氢杨梅素对肝纤维化大鼠脂质过氧化损伤的保护作用(1)
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[摘要] 目的：观察二氢杨梅素对四氯化碳(CCl4)所致大鼠肝纤维化的保护作用，并探讨与抗脂质过氧化有关的作用机制。方法：84只雄性SD大鼠随机分为正常对照组、模型组、复方鳖甲阳性对照组和二氢杨梅素低、中、高剂量组。采用40% CCl4皮下注射制备大鼠肝纤维化模型，造模的同时，二氢杨梅素低、中、高剂量组分别用25 mg/100 g、50 mg/100 g和100 mg/100 g 3种不同浓度的二氢杨梅素进行干预，持续13周，检测肝组织匀浆丙二醛(MDA)含量以及超氧化物歧化酶(SOD)活性变化，光镜下观察肝组织病理学变化。结果：二氢杨梅素可明显降低肝纤维化时升高的MDA含量(P<0.05)；升高肝纤维化时降低的SOD水平(P<0.05)；光镜下观察模型组大鼠肝细胞严重变性、坏死，胶原纤维明显增加，二氢杨梅素各剂量组大鼠肝细胞病理损伤得到明显改善。结论：二氢杨梅素对CCl4所致的大鼠肝纤维化有明显的保护作用，其机制可能与抗脂质过氧化损伤有关。
[关键词] 二氢杨梅素；肝纤维化；脂质过氧化；丙二醛；超氧化物歧化酶
[中图分类号] R575[文献标识码]A [文章编号]1673-7210(2009)06(c)-026-03
Protective effects of dihydromyricetin on lipid peroxidation in rats with hepatic fibrosis
KUANG Manyuan, LUO Mingying, JIA Lei
(Department of Anatomy, Xiangnan College, Chenzhou 423000, China)
[Abstract] Objective: To observe the protective effects of dihydromyricetin on hepatic fibrosis in rats induced by carbon tetrachloride (CCl4), and explore its mechanism related to anti-lipid peroxidation in rats. Methods: 84 male SD rats were randomly divided into six groups: normal group, model group, Fufangbiejia positive control group, lower, middle and high dosages of dihydromyricetin treatment groups. The hepatic fibrosis rat model was developed by subcutaneous injecting 40% CCl4. At the same time, rats were treated with dihydromyricetin at 25 mg/100 g, 50 mg/100 g or 100 mg/100 g. The levels of malondialdehyde (MDA) and superoxide dismutase (SOD) activities in liver tissue were determined, the histopathological change of the liver tissues was observed under optical microscope. Results: Dihydromyricetin could decrease serum level of MDA obviously (P<0.05), which were increased in fibrotic group; and increased the level of SOD in hepatic tissues obviously (P<0.05), which was depressed in fibrotic group. The degeneration and necrosis level of hepatocytes and the distribution of collagen fibrosis were markedly increased in the model group. Dihydromyricetin could significantly alleviate pathological changes and the collagen fibrosis. Conclusion: Dihydromyricetin has good protective effects on hepatic fibrosis induced by CCl4. Its mechanism may be correlated with its anti-lipid peroxidation ......
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