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作 者:王旭焘 潘定一[1] 郭玮 陈思思 周斌[1] 杨钧杰[1] 齐敏友[1]
机构地区:[1]浙江工业大学药学院药理学教研室,杭州310014
出 处:《中国应用生理学杂志》2017年第6期564-567,共4页Chinese Journal of Applied Physiology
基 金:浙江省自然科学基金(LY16H280013);浙江省科技厅新苗人才计划(2015R403050);浙江工业大学大学生创新创业训练计划(2017094)
摘 要:目的:研究阿魏酸(FA)对链脲佐菌素(STZ)致糖尿病大鼠肾脏足细胞损伤的影响,并探讨其可能的机制。方法:雄性SD大鼠尾静脉一次性注射STZ(40 mg/kg,i.v.),72 h后将血糖高于16.7 mmol/L者视为糖尿病造模成功,将其随机分为模型组、阿魏酸组,每组10只;另取10只雄性SD大鼠作为对照组;阿魏酸组(100 mg/kg,i.g.,qd),从大鼠血糖升高第5周开始给药,连续8周。测定空腹血糖、体重、肾脏脏器系数、血清尿素氮、肌酐含量;HE染色观察肾组织病理变化;免疫组化测定肾组织nephrin、podocin蛋白表达。结果:与对照组比较,模型组肾脏脏器系数增大,肾功能下降;病理学显示肾脏细胞萎缩,排列不整齐,并伴有间质增生;足细胞nephrin、podocin蛋白表达明显减少,阿魏酸组明显改善上述指标。结论:阿魏酸具有改善STZ致糖尿病大鼠肾脏功能的作用,其机制可能与上调肾脏足细胞nephrin、podocin蛋白表达有关。Objective: To investigate the effects of ferulie acid (FA) on the streptozocin (STZ) -induced kidney injury in diabetic rats and its possible mechanisms. Methods: Diabetes was induced in male SD rats by an injection of STZ (40 mg/kg, i. v. ). After 72 hours, blood glucose levels were detected and blood glucose levels exceeded 16.7 retool/l, were, diagnosed as dialytic model rats. Diabetic model rats were randomly divided into model group and FA group, ten animal in each group. Another 10 healthy male SD rats were treated as control group. The rats in FA group were treated with FA ( 100 mg/kg, i.g., qd ) from the 5th week since the diabetic rats model was successfully established and lasted for 8 weeks. The levels of blood glucose, body weight, organ coefficient of kidney, blood urea nitrogen and creatinine were tested. HE staining was employed to observe the pathological changes of the renal tissue. Inununohistochemistry was employed to determine the protein of nephrin and podocin. Results: Compared to control group, the levels of blood glucose, organ coefficient of kidney, blood urea nitro- gen(BUN) and serum creatitfine(sCr) were increased significantly. Renal cells from model group rats showed atrophied and disordered after HE staining and interstitial proliferation were 'also appeared in renal tissue of the model group. Meantime, the levels of nephrin and podoein protein were obviously decreased. These changes were significantly attenuated in the model group treated with FA. Conclusion: FA can evidently ameliorate renal damage in rats with diabetic nephropathy induced by STZ, which might be related to increase the level of nephrin and podocin protein.
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