中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2014年
3期
597-599
,共3页
文冰%韩辉%焦周阳%刘超%夏冰%赵文增
文冰%韓輝%焦週暘%劉超%夏冰%趙文增
문빙%한휘%초주양%류초%하빙%조문증
缺血再灌注损伤%曲美他嗪%炎性反应
缺血再灌註損傷%麯美他嗪%炎性反應
결혈재관주손상%곡미타진%염성반응
Ischemia reperfusion injury%Trimetazidine%Inflammation
目的 探讨曲美他嗪(TMZ)抗大鼠心肌缺血再灌注损伤中炎性反应的作用及其机制.方法 雄性健康成年SD大鼠24只,体质量为180～220 g.采用随机区组设计将大鼠随机分为对照组(A组)和TMZ组(B组),B组于实验前6d,每日给予生理盐水稀释的TMZ 10 mg/kg灌胃,各组均采用冠状动脉结扎法制作缺血再灌注损伤(IRI)模型,缺血30 min,再灌注90 min.分别于缺血前、再灌注30、60、90 min后,取大鼠静脉血2ml,测血浆肿瘤坏死因子-α(TNF-α)的含量,实验结束后处死大鼠,再灌注区取组织,免疫组织化学检测血管细胞黏附分子1(VCAM-1)表达.结果 对照组缺血前、再灌注后30、60、90 min血清TNF-α含量分别为(0.18 ±0.10)、(1.15 ±0.29)、(0.98±0.27)、(0.52±0.23) μg/L,TMZ组TNF-α含量在再灌注各测试时点[(0.16±0.12)、(0.87±0.22)、(0.73±0.32)、(0.38 ±0.17) μg/L]均显著低于对照组,差异有统计学意义(P＜0.01);TMZ组与对照组比较,可显著降低心肌组织内VCAM-1(4.571 2±1.121 3比6.203 5±1.451 3)的表达,差异有统计学意义(P＜0.05).结论 TMZ可通过限制再灌注损伤中炎性反应保护大鼠缺血再灌注损伤心肌.
目的 探討麯美他嗪(TMZ)抗大鼠心肌缺血再灌註損傷中炎性反應的作用及其機製.方法 雄性健康成年SD大鼠24隻,體質量為180～220 g.採用隨機區組設計將大鼠隨機分為對照組(A組)和TMZ組(B組),B組于實驗前6d,每日給予生理鹽水稀釋的TMZ 10 mg/kg灌胃,各組均採用冠狀動脈結扎法製作缺血再灌註損傷(IRI)模型,缺血30 min,再灌註90 min.分彆于缺血前、再灌註30、60、90 min後,取大鼠靜脈血2ml,測血漿腫瘤壞死因子-α(TNF-α)的含量,實驗結束後處死大鼠,再灌註區取組織,免疫組織化學檢測血管細胞黏附分子1(VCAM-1)錶達.結果 對照組缺血前、再灌註後30、60、90 min血清TNF-α含量分彆為(0.18 ±0.10)、(1.15 ±0.29)、(0.98±0.27)、(0.52±0.23) μg/L,TMZ組TNF-α含量在再灌註各測試時點[(0.16±0.12)、(0.87±0.22)、(0.73±0.32)、(0.38 ±0.17) μg/L]均顯著低于對照組,差異有統計學意義(P＜0.01);TMZ組與對照組比較,可顯著降低心肌組織內VCAM-1(4.571 2±1.121 3比6.203 5±1.451 3)的錶達,差異有統計學意義(P＜0.05).結論 TMZ可通過限製再灌註損傷中炎性反應保護大鼠缺血再灌註損傷心肌.
목적 탐토곡미타진(TMZ)항대서심기결혈재관주손상중염성반응적작용급기궤제.방법 웅성건강성년SD대서24지,체질량위180～220 g.채용수궤구조설계장대서수궤분위대조조(A조)화TMZ조(B조),B조우실험전6d,매일급여생리염수희석적TMZ 10 mg/kg관위,각조균채용관상동맥결찰법제작결혈재관주손상(IRI)모형,결혈30 min,재관주90 min.분별우결혈전、재관주30、60、90 min후,취대서정맥혈2ml,측혈장종류배사인자-α(TNF-α)적함량,실험결속후처사대서,재관주구취조직,면역조직화학검측혈관세포점부분자1(VCAM-1)표체.결과 대조조결혈전、재관주후30、60、90 min혈청TNF-α함량분별위(0.18 ±0.10)、(1.15 ±0.29)、(0.98±0.27)、(0.52±0.23) μg/L,TMZ조TNF-α함량재재관주각측시시점[(0.16±0.12)、(0.87±0.22)、(0.73±0.32)、(0.38 ±0.17) μg/L]균현저저우대조조,차이유통계학의의(P＜0.01);TMZ조여대조조비교,가현저강저심기조직내VCAM-1(4.571 2±1.121 3비6.203 5±1.451 3)적표체,차이유통계학의의(P＜0.05).결론 TMZ가통과한제재관주손상중염성반응보호대서결혈재관주손상심기.
Objective To investigate the protective effects and mechanism of trimetazidine (TMZ) on inflammation among myocardial ischemia reperfusion injury in rat.Methods Experiments were performed on adult male SD rats weighing 180-220 g.They were randomly divided into two groups:the control group (A) and the TMZ treated group (B).Before establishment of ischemia reperfusion model,rats in group B were fed with 10 mg/kg TMZ for six days.Myocardial ischemia-reperfusion injury models were made by ligating the coronary artery for 30 min followed by reperfusion for 90 min.Venous blood was collected before ischemia and at 30,60,90 min after reperfusion,and then,tumor necrosis factor (TNF-α) was detected.After experiment,rats were executed and tissue samples were removed from IR areas.The expression of intercellular adhesion molecule-1 (ICAM-1) was investigated by employing immunohistochemical method in the tissue samples.Results As compared with the group A,the level of TNF-α in blood plasma after reperfusion (30,60,90 min) was decreased significantly [(1.15 ± 0.29),(0.98 ±0.27),(0.52 ±0.23) μg/L vs.(0.87 ±0.22),(0.73 ±0.32),(0.38 ±0.17) μg/L,P ＜0.01),and the express of vascular cell adhesion molecule-1 (VCAM-1) in myocardial tissue was decreased significantly (6.203 5 ± 1.451 3 vs.4.571 2 ± 1.121 3,P ＜ 0.05) in group B.Conclusion Trimetazidine has notable protective effect on myocardial ischemia reperfusion injury through limiting the inflammation.
