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作 者:吴衡生[1] 王宏伟[1] 徐钦儒[1] 刘桐林 匡裕久
机构地区:[1]同济医科大学附属同济医院儿科,武汉430030
出 处:《同济医科大学学报》1997年第5期384-386,共3页Acta Universitatis Medicinae Tongji
摘 要:建立家兔系膜增殖性肾炎模型,研究API0134对家兔血脂、超氧歧化酶(SOD)及丙二醛(MDA)作用以及对肾脏组织的影响,并探讨了可能的机制。结果表明,API0134用药组血清总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)低于模型组,高密度脂蛋白胆固醇(HDL-C)及HDL-C/LDL-C高于模型组(P<0.05),SOD活性明显高于模型组(P<0.01),而MDA正常。用药组肾组织损害较轻。研究证实,API0134能够预防兔的高脂血症,具有抗氧化作用,能够抑制系膜细胞及基质的增殖,保护肾组织。Rabbit mesangial proliferative glomerulonephritis model was established to investigate the effects of API0134 on the levels of blood-lipid, superoxide dismutase (SOD) and molondialdehyde (MDA), and on the kidney tissues. Their mechanism was also explored. The results demonstrated that the levels of serum total cholesterol (TC), triglyceride (TG) and low density lipoprotein cholesterol (LDL-C) in API0134 group were lower than those in model group (P<0. 05), while the ratio of high density lipoprotein (HDL-C) to LDL-C in API0134 group was obviously higher than that in model group (P<0. 01). The level of MDA was normal. The kindey lesions in API0134 group were significantly alleviated. It was suggested that API0134 might effectively prevent experimental hyperlipidemia, have anti-oxygenating effect, inhibit the proliferation ofmesangial cells and protect the kidney tissues from being injured in rabbit.
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