文章摘要
王强钟丽华于雷卢宝玲汪云朱丽影△.藏红花对肝纤维化大鼠肝组织TGF-β1 表达的影响[J].,2012,12(17):3228-3231
藏红花对肝纤维化大鼠肝组织TGF-β1 表达的影响
Effects of Zanghonghua on Expression of Transforming GrowthFactors-β1 in Rats with Liver Fibrosis
  
DOI:
中文关键词: 肝纤维化  藏红花  TGF-β1  大鼠
英文关键词: Liver fibrosis  Zanghonghua  TGF-β1  Rats
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作者单位
王强钟丽华于雷卢宝玲汪云朱丽影△ 哈尔滨医科大学附属第四医院 
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中文摘要:
      目的:通过观察藏红花对肝纤维化大鼠肝组织TGF-β1 表达的影响,探讨藏红花预防肝纤维化作用的机制。方法:清洁级 SD 雄性大鼠60 只随机分为正常组、模型组、藏红花组、丹参组,每组十五只。应用30%四氯化碳橄榄油溶液3ml/kg·腹腔注射制 备肝纤维化大鼠模型。治疗8 周后,通过HE 和Masson 染色观察肝纤维化的形成、免疫组化检测肝组织中TGF-β1 蛋白的表达。 结果:臧红花组、丹参组与模型组相比肝纤维化程度均轻于模型组(P<0.01),而藏红花组与丹参组相比肝纤维化程度无显著性差 异(P>0.05),臧红花组、丹参组与模型组相比TGF-β1 蛋白的表达均明显减少,而藏红花组与丹参组相比TGF-β1 蛋白的表达没有 显著性差异(P>0.05)。结论:藏红花能有效减轻肝纤维化大鼠的肝脏损伤及纤维化程度,其机制可能与抑制肝内TGF-β1 的表达, 抑制HSC 的激活以及阻断HSC 与TGF-β1 之间的恶性循环有关。
英文摘要:
      Objective: To investigate the mechanism of Zanghonghua to prevent hepatic fibrosis by detect the effects of Zanghonghua on Expression of Transforming Growth Factorsβ1 in Rats with Liver Fibrosis. Methods: Sixty male rats of clean grade were divided into groups marked "normal", "model", "Zanghonghua" and "Danshen", each group is fifteen. Liver fibrosis models of bandicoots were given 30% carbon tetrachloride solution of 3ml/kg·olive oil by intraperitoneal injection.After eight weeks of medical treatment, hepatic fibrosis was detected by using HE and Masson pigmentation, immuno-histochemistry checking of TGF-β1 protein expression in hepatic tissue. Results: The degree of liver fibrosis of those groups that marked "Danshen" and "Zanghonghua" were lighter than the models (P<0.01), but the degree of liver fibrosis showed no difference between the Danshen group and Zanghonghua group (P>0.05). The expression of TGF-β1 protein reduced clearly in the Danshen group and Zanghonghua group, as compared with models, it showed no difference between the Danshen group and Zanghonghua group(P>0.05). Conclusions: Zanghonghua had effects on easing the liver damage and hepatic fibrosis condition of bandicoots. The mechanism may be relative to the restraining of TGF-β1 expression inside the liver, retreat the HSC activation and block the Vicious cycle between HSC and TGF-β1.
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