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机构地区:[1]镇江市中西医结合肾脏病研究所,江苏镇江212028
出 处:《中国中西医结合急救杂志》2006年第3期150-152,F0003,共4页Chinese Journal of Integrated Traditional and Western Medicine in Intensive and Critical Care
基 金:江苏省镇江市临床重点学科基金资助项目(2004282)
摘 要:目的:探讨中药肾炎康治疗大鼠系膜增生性肾炎(M sPGN)的机制。方法:采用大鼠慢性血清病性M sPGN模型。于制模第6周起,肾炎康组每日灌服肾炎康口服液3 m l,模型组每日灌服等量自来水;给药42 d后,测定24 h尿蛋白定量、尿中肿瘤坏死因子α(TNFα)、内皮素1(ET 1)及肾功能,光镜下观察肾组织病理学改变。结果:模型组24 h尿蛋白、尿中TNFα、ET 1及尿素氮(BUN)、血肌酐(SC r)均显著高于正常对照组大鼠(P均<0.01);光镜下肾小球增大,弥漫性系膜增生,节段性加重,肾小球内有较多细胞浸润,肾小管有不同程度的上皮细胞浊肿及脱落,间质亦有一定程度的炎性改变。肾炎康组24 h尿蛋白、尿中TNFα、ET 1及BUN、SC r均显著低于模型组(P<0.05或P<0.01);肾脏组织病理改变较轻,系膜细胞轻度增生或呈节段性增生,肾小管病变轻微。结论:肾炎康通过抑制肾内TNFα及ET 1的合成,抑制系膜细胞增殖及肾小管间质的病理损伤,从而减少蛋白尿,保护肾功能。Objective. To investigate the mechanism of Shenyankang (肾炎康)on rats with mesangial proliferative glomerulonephritis (MsPGN). Methods: MsPGN rat model was induced by chronic serum-sickness. Six weeks later, MsPGN rats were given 3 ml of Shenyankang oral liquor every day (Shenyankang oral liquor treated group) or 3 ml of water every day (model group). Forty-two days after using the drug, urine protein (UP) of 24 hours, renal function and urine level of tumor necrosis factor-(TNF-α) and endothelin-1 (ET-1) were evaluated. Pathologic changes of renal tissue were observed by microscopy. Results: Compared to the normal control group, UP of 24 hours, blood urea nitrogen (BUN), serum creatinine (SCr) and urine level of TNF-α and ET-1 increased significantly in model group (all P〈0.01). Renal tissue pathologic changes were also apparent in model group. The pathological manifestations of the model group were enlarged glomeruli, diffuse mesangial proliferation with segmental severity, inflammatory cell infiltration and tubular epithelial cell lesions. Shenyankang oral liquor treatment significantly decreased UP of 24 hours, BUN, SCr and urine level of TNF-α and ET-1, and improved renal tissue pathological changes, which showed mild or segmental proliferation of mesangial cells and mild changes of renal tubules. Conclusion: Shenyankang oral liquor shows its effect of lowering UP, improving renal function and renal tissue pathology through inhibiting the production of renal TNF-α, ET-1, the proliferation of mesangial cells and the pathologic injury of renal tubules in MsPGN rats.
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