摘要
目的:观察参附注射液(shenfuinjection,SF)对肾缺血再灌注损伤大鼠P38丝裂原活化蛋白激酶(P38MAPK)、肿瘤坏死因子-α(TNF-α)、细胞间粘附分子-1(ICAM-1)表达的影响,并探讨其肾脏保护作用的可能机理。方法:动物随机分为假手术对照组、缺血再灌注组、参附预处理组3组。免疫组化法检测肾组织P38MAPK、ICAM-1蛋白含量,酶联免疫吸附实验(ELISA)检测肾组织和血浆TNF-α的表达。结果:缺血再灌注组P38MAPK、ICAM-1表达和TNF-α含量明显高于假手术对照组(P<0.01)。与缺血再灌注组相比,参附组P38MAPK、ICAM-1表达和TNF-α含量明显降低(P<0.01)。结论:SF可能通过抑制P38MAPK的表达,从而下调TNF-α、ICAM-1的表达,发挥其肾脏保护作用。
AIM： To explore protective and therapeutic effects of the shenfu injection （SF） against renal ischemia repeffusionand anti its possible mechanisms by studying the impact of SF on P38 mitogen activated protein kinase （P38MAPK）, tumor necrosis factor alpha （TNF-α） and intercellular adhensive molecule-1 （ICAM- 1 ）. METHODS： 36 male SD rats were randomly divided into control group, isehemia reperft, sion （IR） group and SF group. Rats were subjected to lefl renal pediele occlusion followed by repeffusion with contralateral nephreetomy. The expression of P38MAPK and ICAM-1 were evaluated by Imunohistochemistrv. The expression of TNF-α in the kidney tissue and plasma were analvzed by enzymlinked immunoadsordent assay （ELISA）. RESULTS： The expression of P38MAPK and ICAM-1, concentration of TNF-a in IR group were higher than that in the control group （P 〈 0.01）. The expression of P38MAPK and ICAM-1, and concentration of TNF-α in SF group were lower than that in the IR group （ P 〈 0.01 ）. CONCLUSION： The SF injection can downregulate the expression of TNF-α and ICAM-1 through inhibiting P38MAPK. SF has an important role in a renoprotective therapeutic regimen.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2005年第8期943-946,共4页
Chinese Journal of Clinical Pharmacology and Therapeutics
作者简介
孙艳玲，女，主治医师，硕士研究生，主要从事麻醉与器官保护工作.Tel：（0）13872809376 E-mail：sysy12005@126．com
刘先义，通讯作者，男，主任医师，教授，硕士生导师，研究方向为器官保护。Tel：（O）13507117487 E-mall：whxy12005@126．com
