上海医学
上海醫學
상해의학
SHANGHAI MEDICAL JOURNAL
2001年
2期
85-88
,共4页
周同%李晓%宋巍%吴佩%张东华%张明均%陈楠%董德长
週同%李曉%宋巍%吳珮%張東華%張明均%陳楠%董德長
주동%리효%송외%오패%장동화%장명균%진남%동덕장
肾缺d再灌注损伤%P-选择素%细胞间粘附分子-1%自由基%细胞凋亡
腎缺d再灌註損傷%P-選擇素%細胞間粘附分子-1%自由基%細胞凋亡
신결d재관주손상%P-선택소%세포간점부분자-1%자유기%세포조망
目的探讨粘附分子P-选择素和细胞间粘附分子-1(ICAM-1)在肾缺d再灌注损伤中的作用,以及P-选择素单克隆抗体的阻断意义。方法建立肾缺d再灌注损伤大鼠模型,观察P-选择素单抗处理前后的大鼠肾组织中P-选择素及ICAM-1表达,及其丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性和细胞凋亡等变化。结果缺d再灌注后,大鼠肾组织中P-选择素和ICAM-1先后明显表达,且MDA含量增加和SOD活性下降,出现明显的细胞凋亡及组织学病理改变。经给予P-选择素单抗处理,肾组织中P-选择素和ICAM-1表达受到抑制,MDA含量降低和SOD活性增高,细胞凋亡减少及组织学病理改变减轻。结论粘附分子P-选择素和ICAM-1参与了肾缺d再灌注损伤机制,以单抗抑制P-选择素可明显减少肾内炎症细胞浸润,脂质过氧化反应,细胞凋亡及组织损伤。
目的探討粘附分子P-選擇素和細胞間粘附分子-1(ICAM-1)在腎缺d再灌註損傷中的作用,以及P-選擇素單剋隆抗體的阻斷意義。方法建立腎缺d再灌註損傷大鼠模型,觀察P-選擇素單抗處理前後的大鼠腎組織中P-選擇素及ICAM-1錶達,及其丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性和細胞凋亡等變化。結果缺d再灌註後,大鼠腎組織中P-選擇素和ICAM-1先後明顯錶達,且MDA含量增加和SOD活性下降,齣現明顯的細胞凋亡及組織學病理改變。經給予P-選擇素單抗處理,腎組織中P-選擇素和ICAM-1錶達受到抑製,MDA含量降低和SOD活性增高,細胞凋亡減少及組織學病理改變減輕。結論粘附分子P-選擇素和ICAM-1參與瞭腎缺d再灌註損傷機製,以單抗抑製P-選擇素可明顯減少腎內炎癥細胞浸潤,脂質過氧化反應,細胞凋亡及組織損傷。
목적탐토점부분자P-선택소화세포간점부분자-1(ICAM-1)재신결d재관주손상중적작용,이급P-선택소단극륭항체적조단의의。방법건립신결d재관주손상대서모형,관찰P-선택소단항처리전후적대서신조직중P-선택소급ICAM-1표체,급기병이철(MDA)함량、초양화물기화매(SOD)활성화세포조망등변화。결과결d재관주후,대서신조직중P-선택소화ICAM-1선후명현표체,차MDA함량증가화SOD활성하강,출현명현적세포조망급조직학병리개변。경급여P-선택소단항처리,신조직중P-선택소화ICAM-1표체수도억제,MDA함량강저화SOD활성증고,세포조망감소급조직학병리개변감경。결론점부분자P-선택소화ICAM-1삼여료신결d재관주손상궤제,이단항억제P-선택소가명현감소신내염증세포침윤,지질과양화반응,세포조망급조직손상。
Objective To investigate the role of P-selectin and intercellular adhesive molecule-1 (ICAM-1) inrenal ischemia-reperfusion injury, as well as the preventive effect of anti-P-selectin monoclonal antibody (mAb).Method P-selectin and ICAM-1 expression in renal tissue, cell apoptosis, MDA contents and SOD activities were detected in rat model of renal ischemia-reperfusion injury. Some ischemia-reperfusion rats were treated with anti-P-selectin mAb. Resalts Histopathologic damage, up-regulated expression of P-selectin and ICAM-1, cell apoptosis, increased MDA contents and declined SOD activities were found in renal tissues following renal ischemia-reperfusion injury, while these changes became less conspicuous in animal treated with anti-P-selectin mAb. Couclusian P-selectinand ICAM-1 might mediate inflammatory cell infiltration, cell apoptosis and lipid peroxidation and contribute to renalischemia-reperfusion injury, which could be inhibited by the anti-P-selectin mAb. (Shanghai Med J, 2001,24:85-88)