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机构地区:[1]重庆医科大学附属第二医院内分泌科,400010
出 处:《重庆医学》2009年第19期2463-2464,2467,共3页Chongqing medicine
摘 要:目的观察探讨糖尿病大鼠肝组织内CTGF的表达情况以及辛伐他汀干预对表达的可能影响和机制。方法雄性SD大鼠随机分为2组,A组(正常对照组)10只,B组20只。B组:STZ按50mg/kg体质量腹腔内单次注射,作为糖尿病模型组。药物注射72h后,两组大鼠均取尾静脉血测血糖,血糖值大于16.7mmol/L者确定为糖尿病大鼠模型。A组大鼠血糖均正常,B组所有大鼠均符合糖尿病大鼠模型标准。再将B组随机分为B1组(糖尿病对照组)和B2组(辛伐他汀治疗组),每组10只。B2组以辛伐他汀5mg·kg-1.d-1干预,A、B1组均予等量生理盐水对照。14W后测体质量、空腹血糖、血脂(TC、TG)。肝组织HE染色做病理检查,CTGF免疫组织化学法采用SABC技术。结果与A组相比,B1组体质量明显下降,血糖、TG、TC明显升高(P<0.05),B2组对体质量、血糖及TG无明显影响,降低TC(P<0.05)。光镜下:B1组部分肝组织结构紊乱,可见脂滴空泡;B2组肝组织结构较清晰,亦可见散在脂滴空泡。免疫组织化学法检测:B2组肝组织CTGF表达明显增加(P<0.05);B2组CTGF表达较B1组减少(P<0.05)。结论糖尿病肝损害早期就存在CTGF表达增加,氧化应激可能在其中起着重要作用。给药组CTGF表达减少,可能是通过抗氧化作用减低了氧化应激,抑制了HSC的活化。Objective To study effects and mechanisms of simvastatin on connective tissue growth factor expression in the liver of diabetic rats. Methods Rats were randomly divided into group A(10 rats) and group B(20 rats). Diabetes group B were induced by injection of streptozotocin successfully and then were randomly separated into group B1 and group B2. Group B2 were treated with simvastatin. 14 weeks later, Liver lesions were evaluated using HE staining. Immunohistochemistry for CTGF was performed by SABC technique. Results To contrast with group A, the decline in body weight and rise in plasma glucose,TC and TG were significant(P〈0.05), simvastatin could prevent the rise of TC significantly(P〈0.05) ,hut not prevent the decline in body weight and rise in plasma glucose and TG. Light microscopy in HE staining showed that Part of the organizational structure of the model group liver was in disorder,and some lipid vacuoles could be seen. But the same changes were ont observed in simvastatin group. Liver from model group presented the CTGF expression was increased significantly compared with the group A(P〈0.05) ,and simvastatin administration reduced this change(P〈0.05). Conclusion The CTGF expression is increased significantly in the early stage of liver injury in diabetic rats,and oxidative stress may be an important role. The mechanism of simvastatin effects may be correlated with suppression on oxidative stress in liver in diabetic rats.
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