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目的:探讨非促分裂型人酸性成纤维细胞生长因子(nm-haFGF)对大鼠肾缺血再灌注损伤的影响。方法:摘除大鼠左侧肾脏,随即夹毕大鼠右侧肾动脉60 min,24 h后松开动脉夹,建立肾缺血再灌注损伤模型。再灌注后5 min后,经舌静脉注射不同剂量的nm-haFGF,并用haFGF作为对照。24 h后取大鼠肾组织、血液和尿液,检测肾脏组织和血液中SOD、MDA以及血液和尿液中BUM、Cr的变化,并进行肾组织病理学检测。结果:缺血再灌注24 h后,nm-haFGF所有剂量组和haFGF组血清SOD活性明显高于模型组,MDA含量明显低于模型组,而血清和尿BUN和Cr含量均明显低于模型组;肾组织SOD活性在nm-haFGF 20μg/kg和40μg/kg剂量组和haF-GF组明显升高而MDA含量明显降低。组织学检查结果显示,nm-haFGF可明显减轻缺血再灌注引起的肾组织水肿,肾小管刷状缘脱落和细胞坏死。结论:nm-haFGF可拮抗肾缺血再灌注引起的损伤。
Objective: To investigate the effect of non-mitogenic human acidic fibroblast growth factor (nm-haFGF) on renal ischemia-reperfusion injury in rats. Methods: The left kidney of the rats was removed, then the right renal artery of rats were sacrificed for 60 min, then the artery clamp was released 24 h later to establish the model of renal ischemia-reperfusion injury. Five minutes after reperfusion, different doses of nm-haFGF were injected via the lingual vein, and haFGF was used as a control. Twenty-four hours later, the kidneys, blood and urine were collected and the changes of SOD, MDA, BUM and Cr in blood and urine were measured and the pathological changes of renal tissue were detected. Results: After 24 h of ischemia-reperfusion, the serum SOD activity in all the groups of nm-haFGF and haFGF was significantly higher than that of the model group, the content of MDA was significantly lower than the model group, but the serum and urine BUN and Cr levels were significantly lower than the model group ; The activity of SOD in renal tissue was significantly increased and the content of MDA was significantly decreased in the groups of 20μg / kg and 40μg / kg of nm-haFGF and haF-GF. Histological examination showed that, nm-haFGF can significantly reduce ischemia-reperfusion induced renal tissue edema, brush border detachment and cell necrosis. Conclusion: nm-haFGF can antagonize the injury induced by renal ischemia-reperfusion.