论文部分内容阅读
目的:探讨溺毒清合剂延缓慢性肾衰竭的作用机制。方法:采用5/6肾切除造模方法复制大鼠慢性肾衰竭模型,实验分为假手术组、模型组、溺毒清低剂量组(简称溺低组)、溺毒清高剂量组(简称溺高组)、厄贝沙坦对照组(简称厄贝组)。对各组进行干预治疗,然后观察其肾功能变化。并进行血清超氧化物歧化酶(SOD)、丙二醛(MDA)、一氧化氮(NO)、一氧化氮酶(ET-1)检测,并对肾组织经行Ⅳ胶原、纤维连接蛋白(FN)、基质金属蛋白酶-2(MMP-2)、转化生长因子-β(TGF-β)等免疫组化检测,最后行肾组织病理检查。结果:溺毒清合剂可显著降低CRF大鼠ET-1,升高NO,对MDA、SOD差异无统计学意义,改善肾功能方面与厄贝沙坦相当。免疫组化显示溺毒清高剂量组比模型组Ⅳ胶原、FN、TGF-β表达减少。结论:溺毒清合剂可显著改善CRF大鼠的肾功能,可能与其改善肾血流,降低血浆ET-1升高NO水平,从而抑制肾小球系膜细胞及间质细胞增值,通过降解Ⅳ型胶原等细胞外基质而抑制5/6肾切除大鼠残肾组织肾小球硬化,从而延缓慢性肾衰竭进展,与厄贝沙坦有相近的肾脏保护作用。
Objective: To explore the mechanism of Shenfuqing mixture in delaying chronic renal failure. Methods: The rat model of chronic renal failure was established by 5/6 nephrectomy. The rats were divided into sham operation group, model group, drowning low dose group (drowning low group), drowning high dose group High group), irbesartan control group (referred to as Eber group). Each group intervention treatment, and then observe the changes in renal function. The levels of serum SOD, MDA, NO and NO-1 were measured and the expressions of collagen, fibronectin, FN), matrix metalloproteinase-2 (MMP-2), transforming growth factor-β (TGF-β) were detected by immunohistochemistry. Results: Drunking mixture can significantly reduce the ET-1 CRF rats, increased NO, no significant difference between MDA and SOD, and improve renal function and irbesartan quite. Immunohistochemistry showed that the expression of Ⅳ collagen, FN and TGF-β in model group was lower than that in model group. Conclusion: Drunking qi mixture can significantly improve the renal function of CRF rats, which may be related to its improvement of renal blood flow, decrease of plasma ET-1 and increase of NO level, thereby inhibiting the proliferation of mesangial cells and interstitial cells, through the degradation of Ⅳ Collagen and other extracellular matrix inhibit 5/6 nephrectomized rat renal tissue glomerular sclerosis, thereby slowing the progression of chronic renal failure, and irbesartan have a similar protective effect of the kidneys.