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目的研究高盐对AngⅡ肾脏损伤SD大鼠血压、肾脏组织形态、超微结构以及肾脏骨调素(OPN)表达的影响。方法选取12周龄正常盐饮食雄性SD大鼠36只制作AngⅡ(每分钟给予100ng/kg·b.w.)肾脏损伤模型。之后随机分为高盐(4%NaCl)及正常盐(0.6%NaCl)饮食组(n=18)作为对照组。每2周测量大鼠鼠尾血压,分别于AngⅡ输注2周末及不同盐饮食第12周末每组处死6只。采用免疫组化方法测定大鼠肾脏OPN、TGF-β1表达;荧光定量PCR方法测定大鼠肾脏OPNmRNA表达。光镜下观察肾脏组织形态改变,电镜下观察肾脏超微结构改变。结果输注AngⅡ2周后大鼠血压显著升高,大鼠肾脏TGF-β1、OPNmRNA及其蛋白表达升高,与对照组大鼠比较有显著差异(P<0.05)。停用AngⅡ后大鼠血压恢复正常。继续摄入高盐或正常盐饮食,两组大鼠血压无明显差异(P>0.05)。摄入高盐饮食12周后大鼠肾脏TGF-β1、OPNmRNA及其蛋白表达显著升高,与正常盐饮食及对照组大鼠比较,有显著差异(P<0.01)。形态学观察发现输注AngⅡ对大鼠肾脏造成轻度损伤,继续摄入高盐加重大鼠的肾脏损伤。结论AngⅡ肾脏损伤基础之上,高盐摄入加重了大鼠肾脏损伤,高盐所致大鼠肾脏损伤不依赖于血压升高。OPNmRNA及其蛋白表达增强是肾脏损伤的结果。
Objective To investigate the effect of high salt on blood pressure, renal tissue morphology, ultrastructure and osteopontin (OPN) expression in kidney of AngⅡ-injured SD rats. Methods Thirty-six male Sprague-Dawley rats, 12-week-old normal saline diet, were given AngⅡ (100ng / kg · b · w · min) as a model of renal injury. The rats were randomly divided into high salt (4% NaCl) and normal saline (0.6% NaCl) diet groups (n = 18) as control group. Rat tail blood pressure was measured every 2 weeks and 6 rats were sacrificed in each group at the end of the two weeks of Ang II infusion and the end of the twelfth week of different salt diet. The expression of OPN and TGF-β1 in rat kidneys were detected by immunohistochemical method. The expression of OPN mRNA in rat kidney was detected by real-time quantitative PCR. The morphological changes of kidney were observed under light microscope and the ultrastructure of kidney was observed under electron microscope. Results After 2 weeks of Ang Ⅱ infusion, the blood pressure of rats increased significantly, and the expression of TGF-β1, OPN mRNA and protein in rat kidney increased significantly compared with that in the control group (P <0.05). Blood pressure returned to normal after Ang Ⅱ withdrawal. Continue to intake of salt or normal salt diet, the two groups of rats no significant difference in blood pressure (P> 0.05). The expression of TGF-β1, OPNmRNA and protein in rat kidney after ingestion of high-salt diet for 12 weeks was significantly higher than that in normal salt diet and control group (P <0.01). Morphological observation found that infusion of AngⅡ caused mild damage to the kidneys of rats, and continued uptake of salt increased severe kidney injury in rats. Conclusion On the basis of Ang ¢ ò kidney injury, high salt intake aggravates the renal injury in rats, and the kidney damage caused by high salt does not depend on the increase of blood pressure. Increased OPN mRNA and its protein expression are the result of kidney damage.