论文部分内容阅读
目的观察别嘌呤醇对高尿酸血症致大鼠肾损害的影响。方法将SD大鼠分为正常组、模型组、别嘌呤醇组。氧嗪酸和尿酸合用造模,别嘌呤醇组同时给大鼠别嘌呤醇灌胃治疗,于2、4周后分别检测各组大鼠血中尿素氮(BUN)、肌酐(Scr)、尿酸(UA),收集24 h尿量并测24 h尿蛋白定量,比较各组肾脏组织切片中转化生长因子-β1(TGF-β1)、α-平滑肌肌动蛋白(α-SMA)的表达。结果治疗4周后,与模型组相比,别嘌呤醇组大鼠血UA、BUN、Scr明显降低(P<0.05),TGF-β1与α-SMA表达明显减少(P<0.05)。结论别嘌呤醇对高尿酸血症大鼠肾损害有明显的治疗作用,机制可能与其阻断UA生成、降低UA水平、减少UA对肾小管上皮细胞功能的损害、抑制或延缓肾组织病变和肾功能损害有关。
Objective To observe the effects of allopurinol on renal damage induced by hyperuricemia in rats. Methods SD rats were divided into normal group, model group and allopurinol group. Alloxan and uric acid combined with modeling, allopurinol group while giving allopurinol treatment of rats, at 2,4 weeks after the rats were measured blood urea nitrogen (BUN), creatinine (Scr), uric acid (UA). The urinary excretion of 24 h was measured and the urine protein of 24 h was measured. The expression of TGF-β1 and α-SMA in each group were compared. Results After 4 weeks of treatment, the levels of UA, BUN and Scr in allopurinol group were significantly decreased (P <0.05) and the expressions of TGF-β1 and α-SMA were significantly decreased (P <0.05). Conclusions Allopurinol has a significant therapeutic effect on renal damage in rats with hyperuricemia, which may be related to its mechanism of inhibiting the formation of UA, decreasing the level of UA, reducing the damage of UA to renal tubular epithelial cells, inhibiting or retarding renal tissue lesions and kidney Functional damage related.