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目的 研究高胆固醇血症在自发性高血压大鼠 (SHR)肾脏损害中的作用及其作用机制。方法 将 1 4只 2 3周龄的SHR随机分在对照组和高胆固醇组 ,后者喂以 4%胆固醇 +1 % 3号胆盐 +7%猪油混合加工成的大鼠饼干。测量每只大鼠的体重、血压、2 4h尿蛋白排泄量、血、尿NO及肾皮质TGFβ1 mRNA的表达 (RT PCR法 )。实验结束时 ,取其肾脏送HE光镜检查及电镜检查。结果 高胆固醇组的尿蛋白排泄高于对照组 ,血、尿NO低于对照组 ,肾皮质TGFβ1 mRNA表达增强。形态学检查发现 ,高胆固醇组大部分肾小球局灶节段硬化 ,小管扩张 ,可见蛋白管型和间质炎症细胞浸润 ;电镜下可见系膜细胞增生和吞噬脂滴。结论 高胆固醇血症加重SHR的肾脏损害可能通过TGFβ1参与的小球硬化途径
Objective To investigate the role of hypercholesterolemia in kidney damage in spontaneously hypertensive rats (SHR) and its mechanism. Methods Twenty-four SHRs of 23 weeks of age were randomized into control and hypercholesterolemic rats, which were fed a rat biscuit processed with 4% cholesterol + 1% bile salt 3 + 7% lard. Body weight, blood pressure, 24 h urinary protein excretion, blood, urine NO, and renal cortical TGFβ1 mRNA expression were measured in each rat (RT PCR). At the end of the experiment, take their kidneys to HE light microscopy and electron microscopy. Results The excretion of urinary protein in hypercholesterol group was higher than that in control group, while the blood and urine NO levels were lower than those in control group. The expression of TGFβ1 mRNA in renal cortex was enhanced. Morphological examination found that most of the high cholesterol group glomerular focal segmental sclerosis, tubular dilatation, visible protein tubular and interstitial inflammatory cell infiltration; electron microscopy showed mesangial cell proliferation and lipid droplets. Conclusion Hypercholesterolemia aggravates the renal damage of SHR possibly through the pathways of glomerulosclerosis involved in TGFβ1