摘要
目的探讨利用亚硝基左旋精氨酸甲酯(L-NAME)建立子痫前期肾脏损伤大鼠模型的方法,并研究synaptopodin在子痫前期大鼠模型肾脏组织中的表达及在蛋白尿形成中的作用。方法选重200—250g SPF级Wistar大鼠20只,随机分为2组:A组正常妊娠组,B组子痫前期组,B组孕期腹腔内连续注射NO合酶抑制剂(L-NAME)。动态监测孕鼠尾动脉血压、24h尿蛋白总量,测量胎鼠重量。观察两组孕鼠肾脏组织学改变,检测孕鼠肾脏synaptopodin mRNA的表达变化。结果 B组孕鼠腹腔内注射L-NAME后孕鼠尾动脉血压和24h尿蛋白总量明显升高,胎鼠体重明显降低,synaptopodin mRNA表达明显降低,与A组相比,差异有统计学意义。且B组孕鼠肾脏组织出现基底膜增厚,系膜细胞增生等病理学改变。结论孕期腹腔内注射L-NAME可诱导孕鼠产生子痫前期血压升高,蛋白尿等临床症状及肾脏损伤的典型病变,且肾脏synaptopodin的表达降低可能参与孕鼠肾脏损伤从而引起大量血浆蛋白漏出形成蛋白尿。
Objective： To establish rat model with preeclampsia by using L- nitro- arginine methyl ester（ L- NAME） and study the relationship between expression of synaptopodin and formation of preeclampsia proteinuria. Methods： 20 SPF Wistar rats weighting 200- 250g were randomly divided into 2 groups： A group： normal pregnancy group; B group： preeclampsia group,pregnancy rats were injected intraperitoneally by NO syntheses inhibitor（ L- NAME） continuously. We dynamic monitored the tail artery blood pressure of pregnant rats and 24h urine protein quantity,measured fetal weight,observed histological changes of the kidney sections from pregnancy rats and detected glomerular expression of synaptopodin by RT- PCR. Results： The blood pressure and 24h total urinary protein of the preeclampsia group after intraperitoneal injection of L- NAME were significantly increased,in contrast,the weight of fetal rats decreased significantly,compared with the normal pregnant group. The differences had statistical significance. We found that kidney sections from rats with preeclampsia had histological changes,for example,thickness of glomerular basement membrane and proliferation of glomerular mesangial cell. Conclusion： L- NAME can induced typical symptoms of preeclampsia and pathological changes of renal injury. Glomerular expression of synaptopodin decreased maybe induce injury of kidney sections from preeclampsia and involve the formation of preeclampsia proteinuria.
出处
《中国优生与遗传杂志》
2014年第3期30-32,F0003,共4页
Chinese Journal of Birth Health & Heredity
