CAJ | 학술논문

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 20 ìg/kg和40 ìg/kg剂量组和haFGF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.
목적:탐토비촉분렬형인산성성섬유세포생장인자(nm-haFGF)대대서.신결혈재관주손상적영향.방법:적제대서좌측신장,수즉협필대서우측신동맥60 min,24 h후송개동맥협,건립신결혈재관주손상모형.재관주후5 min후,경설정맥주사불동제량적nm-haFGF,병용haFGF작위대조.24 h후취대서신조직、혈액화뇨액,검측신장조직화혈액중SOD、MDA이급혈액화뇨액중BUM、Cr적변화,병진행신조직병이학검측.결과:결혈재관주24 h후,nm-haFGF소유제량조화haFGF조혈청SOD활성명현고우모형조,MDA함량명현저우모형조,이혈청화뇨BUN화Cr함량균명현저우모형조;신조직SOD활성재nm-haFGF 20 ìg/kg화40 ìg/kg제량조화haFGF조명현승고이MDA함량명현강저.조직학검사결과현시,nm-haFGF가명현감경결혈재관주인기적신조직수종,신소관쇄상연탈락화세포배사.결론:nm-haFGF가길항신결혈재관주인기적손상.
AIM:To investigate the effect of non-mitogenic human acidic fibroblast growth factor(nm-haFGF)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 aland 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.