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Apelin-13对高血压性肾纤维化的影响及机制研究

发布时间:2018-08-28 16:10
【摘要】:目的探讨血管紧张素受体AT1相关的受体蛋白(APJ)激动剂Apelin-13对高血压性肾纤维化的影响及其机制。方法 12周龄雄性自发性高血压大鼠随机分为对照组、1μg/(kg·d)Apelin-13组、10μg/(kg·d)Apelin-13组、100μg/(kg·d)Apelin-13组;Apelin-13通过尾静脉给药。测量大鼠24 h尿蛋白量、血清肌酐和尿素氮浓度。采用套尾法测量尾动脉收缩压,HE染色和Masson染色观察大鼠肾脏组织学改变,Western blot检测肾脏组织中自噬相关蛋白微管相关蛋白1轻链3(LC3)、Beclin-1和p62的表达。结果与对照组比较,10μg/(kg·d)Apelin-13组、100μg/(kg·d)Apelin-13组以剂量依赖方式降低大鼠收缩压、24 h尿蛋白量、血清肌酐和尿素氮水平、肾脏损伤评分和胶原容积分数(均P0.05),减轻肾小管上皮细胞水肿,减少间质胶原沉积,降低肾间质纤维化程度。10μg/(kg·d)Apelin-13组、100μg/(kg·d)Apelin-13组也以剂量依赖方式增加大鼠肾脏组织中LC3-Ⅱ表达和LC3-Ⅱ/LC3-Ⅰ比值及Beclin-1表达,降低p62表达(均P0.05)。结论 Apelin-13抑制高血压性肾纤维化的进展,其机制可能与Apelin-13抑制细胞自噬有关。
[Abstract]:Objective to investigate the effect and mechanism of angiotensin receptor AT1 associated receptor protein (APJ) agonist Apelin-13 on hypertensive renal fibrosis. Methods 12-week-old male spontaneously hypertensive rats were randomly divided into 1 渭 g / (kg d) Apelin-13 group and 10 渭 g / (kg d) Apelin-13 group. Apelin-13 was administered via tail vein. Urine protein, serum creatinine and urea nitrogen were measured in 24 h rats. The changes of renal histology in rats were observed by HE staining and Masson staining. The expression of autophagy associated protein microtubule-associated protein 1 (LC3), light chain 3 (LC3), Beclin-1 and p62 in renal tissue was detected by Western blot. Results compared with the control group, 10 渭 g / (kg d) Apelin-13 group (100 渭 g / (kg d) Apelin-13) decreased in a dose-dependent manner the levels of urinary protein, serum creatinine and urea nitrogen, renal injury score and collagen volume fraction (P0.05), and alleviated the edema of renal tubular epithelial cells in a dose-dependent manner. The expression of LC3- 鈪,

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