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血管内皮生长因子在大鼠子痫前期模型中的作用
引用本文:陈丹青,吕晓娟,董旻岳,王正平,贺晶. 血管内皮生长因子在大鼠子痫前期模型中的作用[J]. 浙江大学学报(医学版), 2007, 36(1): 84-87
作者姓名:陈丹青  吕晓娟  董旻岳  王正平  贺晶
作者单位:浙江大学医学院,附属妇产科医院,浙江,杭州,310006
基金项目:浙江省卫生厅资助项目;教育部留学回国人员科研启动基金
摘    要:目的:探讨血管内皮生长因子在大鼠子痫前期模型中的作用。方法:选择清洁级W istar大鼠,随机分为两组,每组14只。对照组于妊娠第7天皮下注射生理盐水;亚硝基左旋精氨酸甲酯(L-NAM E)组于妊娠第7天皮下注射一氧化氮合成酶(NOS)抑制剂L-NAM E,每日125 m g/kg体重。两组均于妊娠第8天每天测量大鼠尾动脉血压,若血压增高合并尿蛋白大于或等于( )时,大鼠子痫前期模型确立。同时,测定两组大鼠血小板数值和血清VEGF浓度后,立即处死大鼠测胎鼠及胎盘重量;采用免疫组化法检测胎盘VEGF表达量。结果:L-NAM E组孕鼠出现类似子痫前期特征,表现为血压明显升高至(145.3±4.6)mmHg,尿蛋白含量增加为(814.3±57.5)m g/L,血小板数显著减少至(467.1±76.3)×109/L及胎鼠胎盘重量明显减轻;对照组孕鼠血压(101.4±7.6)mmHg,尿蛋白(398.2±82.3)m g/L,血小板计数(837.20±71.4)×109/L。两组比较差异均有显著性(P均<0.05)。对照组血清VEGF浓度明显大于L-NAM E组[(13.62±3.33 vs 8.71±2.42)ng/L],胎盘中的VEGF表达量对照组也明显高于L-NAM E组[(0.89±0.19 vs 0.58±0.12)OD],差异均有显著性(P<0.01)。结论:大鼠血清VEGF水平降低和胎盘表达VEGF量下降参与子痫前期的发生。

关 键 词:子痫前期/病因学  疾病模型,动物  内皮生长因子/血液  妊娠并发症  血管内皮生长因子  胎盘  妊娠大鼠
文章编号:1008-9292(2007)00-0084-04
收稿时间:2006-03-28
修稿时间:2006-08-01

Effect of vascular endothelial growth factor on pre-eclampsia in pregnant rats
Dan-Qing Chen,Xiao-Juan Lu,Min-Yue Dong,Zheng-Ping Wang,Jing He. Effect of vascular endothelial growth factor on pre-eclampsia in pregnant rats[J]. Journal of Zhejiang University. Medical sciences, 2007, 36(1): 84-87
Authors:Dan-Qing Chen  Xiao-Juan Lu  Min-Yue Dong  Zheng-Ping Wang  Jing He
Affiliation:The Affiliated Obstetrics and Gynecology Hospital, College of Medicine, Zhejiang University, Hangzhou 310006, China. chendq@zju.edu.cn
Abstract:OBJECTIVE: To investigate relationship between the vascular endothelial growth factor (VEGF) and the pathogenesis of pre-eclampsia in pregnant rats. METHODS: Pregnant rats were divided into two groups randomly. Saline solution or L-nitro arginine methyl ester (L-NAME) 125 mg/d was given subcutaneously from day 7 of gestation till establishing pre-eclampsia. Systolic blood pressure, urine protein, platelet count, and weight of pups and placenta were determined. The levels of VEGF in pregnant rats venous serum, placenta and decidual tissue from normal pregnancy and pre-eclampsia rats were detected by ELISA and immunohistochemistry, respectively. RESULT: Pregnant rats which were given L-NAME produced physical signs similar to those of pre-eclampsia, such as increase in systolic blood pressure [(145.3 +/-4.6)mmHg] and urine protein [(814.3 +/-57.5)mg/L], and decrease in platelet count [(467.1 +/-76.3) x 10(9)/L] and weight of pups and placenta. Compared with controls, the intensity of VEGF immunostaining in trophoblast or decidual cells were significantly reduced. The serum levels of VEGF were significantly lower in pre-eclampsia group than in normal pregnancy. CONCLUSION: Decreased serum levels of VEGF and reduced expression of VEGF in placental tissues might in part explain the pathogenesis of pre-eclampsia in pregnant rats.
Keywords:Pre-eclampsia/etiol  Disease models  animal  Endothelial growth factors/blood  Pregnancy complications  Vascular endothelial growth factor  Placenta  Pregnant rat
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