摘要
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。
AIM : To investigate the effect of non - mitogenic human acidic fibroblast growth factor ( nm - haF- GF) on renal ischemia- reperfusion injury in rats. METHODS: Rat renal ischemia- reperfusion (I/R) injury was produced by removing the left kidney and subsequently clamping the right renal artery for 60 min followed by reperfusion for 24 h. 5 min after reperfusion, different doses of nm - haFGF and haFGF ( as positive control) were injected by lingual vein. 24 h later, the samples of blood, urine and kidney were collected and the contents of malondialdehyde (MDA), blood urea nitrogen (BUN), creatinine (Cr) and superoxide dismutase (SOD) activity were detected. Histopathological changes were also observed. RESULTS : In the serum, SOD activity of all the nm - haFGF groups and the haFGF group increased significantly while the content of MDA decreased dramatically compared with the model group; The content of BUN and Cr also decreased wherever in serum or in urine ; In renal tissue, SOD activity in nm - haFGF 20 μg/kg group, 40 μg/kg group and haFGF group rose significantly compared with the model group, while MDA decreased dramatically. Histological examination showed that nm- haFGF markedly attenuates the renal edema, brush border's defluvium and cell necrosis induced by ischemia- reperfusion. CONCLUSION: nm -haFDF could resist the renal injury induced by ischemia- reperfusion in rats.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2008年第3期552-557,共6页
Chinese Journal of Pathophysiology
基金
Supported by National High Technology Research and Development Program of China(863 Program,No.2002AA2Z3318
No.2004AA2Z3C60)