CAJ | 학술논문

目的探讨重组人肿瘤坏死因子受体-IgG1Fc段融合蛋白(rhuTNFR:Fc)对脂多糖(LPS)致大鼠急性肾损伤的保护作用及机制.方法采用静脉注射LPS建立大鼠急性肾损伤模型.Sprague-Dawley大鼠随机分为对照组、rhuTNFR:Fc组、LPS组和rhuTNFR:Fe+LPS组.监测各组大鼠平均动脉压(MAP)变化情况,血液尿素氮(BUN)及肌酐(Cr)水平,观察肾组织病理学改变,同时检测血清TNF-α含量及其生物活性,并测定肾组织丙二醛(MDA)含量、超氧化物歧化酶(SOD)和髓过氧化物酶(MPO)活性.结果 rhuTNFR:Fc预处理能显著降低TNF-αf.生物活性,改善肾功能,减轻LPS所致病理损伤及MPO活力的增高,但对组织MDA含量及SOD活力无明显影响.结论 rhuTNFR:Fc预处理可以部分减轻LPS引起的大鼠急性肾损伤.
목적 탐토중조인종류배사인자수체-IgG1Fc단융합단백(rhuTNFR:Fc)대지다당(LPS)치대서급성신손상적보호작용급궤제.방법 채용정맥주사LPS건립대서급성신손상모형.Sprague-Dawley대서수궤분위대조조、rhuTNFR:Fc조、LPS조화rhuTNFR:Fe+LPS조.감측각조대서평균동맥압(MAP)변화정황,혈액뇨소담(BUN)급기항(Cr)수평,관찰신조직병이학개변,동시검측혈청TNF-α함량급기생물활성,병측정신조직병이철(MDA)함량、초양화물기화매(SOD)화수과양화물매(MPO)활성.결과 rhuTNFR:Fc예처리능현저강저TNF-αf.생물활성,개선신공능,감경LPS소치병리손상급MPO활력적증고,단대조직MDA함량급SOD활력무명현영향.결론 rhuTNFR:Fc예처리가이부분감경LPS인기적대서급성신손상.
Objective To investigate the protective effects of recombinant human tumor necrosis factor receptor:Fc fusion protein (rhuTNFR:Ice)on the acute renal injury induced by lipepelysaccharide(LPS)in rats.Methods Models ofacute renal injury in rats were constructed by intravenous injection of LPS 10 m/kg.Forty-eight SD rats weighing 180～240g were randomly divided into 4 groups with 12 animals each group,including control group,rhuTNFR:Fc group,LPS groupand rhuTNFR:Fc+LPS group.Mean arterial pressure(MAP)wKs continuously monitored for 6 h.The levels of blood tLrea nitrogen(BUN)。Creatinine(Cr),TNF-αas well as TNF-α bioactivity were assessed.The myeloperoxinse(MPO)and superoxide dismutase(SOD)activity,content ofmalondialdehyde(MDA)were also measured.Pathologic changes of lung tissue in each group were observed by HE staining.Results Compared with LPS group,the status of hypotension and pathological manifestation in kidneys were ameliorated,and MPO activity significantly decreased in rhuTNFR:Fc+LPS group(P<0.05).Conclusion These data suggest that rhuTNFR:Fc can ablate the rise in serum TNF-α bioactivity that occurs in response to LPS,and rhuTNFR:Fc could in part protect rats from the acute renal injury induced by LPS.