摘要
目的探讨在系膜增生性肾小球肾炎(M sPGN)中系膜细胞氧化损伤与抗氧化系统的改变及迷迭香酸的干预作用。方法培养大鼠肾小球系膜细胞,以PDGF刺激系膜增生及RAD干预;另外,用兔抗大鼠胸腺细胞免疫血清(ATS),制备大鼠抗THy1.1系膜增生性肾小球肾炎模型,并以迷迭香酸干预。体外及体内实验均设正常对照组、肾炎组、单纯迷迭香酸组和迷迭香酸干预组。利用分光法分别测定培养细胞和肾脏组织中丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性。结果在抗THy1.1肾炎的肾脏组织及PDGF刺激肾小球系膜细胞中MDA含量升高和SOD减少;迷迭香酸的干预后MDA的产生降低,而SOD增加。结论氧自由基及其诱发的脂质过氧化在系膜增生性肾小球肾炎的致病中起重要作用,而迷迭香酸则能抑制肾炎系膜细胞的上述改变,具有抗氧化活性。
Objective To investigate the oxidative damage and the change of antioxidation system in mesangial cells in patients with mesangial proliferative glomerulonephritis （MsPGN） as well as the intervention of rosmarinic acid（RAD）. Method In vitro,rat mesangial ceils were cultured and were stimulated by PDGF to result mesangial proliferation and RAD intervention;in vivo,anti-THy 1.1 serum （ATS） was used in rats to establish an experimental model of anti-THy 1.1 MsPGN, which was intervented by RAD. Both in vitro and in vivo, control group, glomerulonephrit groups without or with RAD were set respectively. The activity of SOD and the content of MDA in cultured ceils and kidney tissue were detected by spectrophotomerty. Results The activity of SOD was found to decrease significantly ,while the content of MDA increased in kidney tissue and PDGF-stimulated mesangial ceils in MsPGN. After intervention of RAD, the content of MDA decreased and SOD increased. Conclusions O2 free radical and lipid peroxidation induced by it play an important role in the etiology of MsPGN. With the activity of antioxidation, RAD can restrain the changes of mesangial cells.
出处
《现代诊断与治疗》
CAS
2006年第5期280-284,共5页
Modern Diagnosis and Treatment
基金
江苏省科委社会发展基金(BS2003050)
南京市社会发展基金(200301093-3)资助
