国际脑血管病杂志
國際腦血管病雜誌
국제뇌혈관병잡지
INTERNATIONAL JOURNAL OF CEREBROVASCULAR DISEASES
2009年
11期
840-843
,共4页
沈丽华%叶民%丁新生%韩秋%吴二兵
瀋麗華%葉民%丁新生%韓鞦%吳二兵
침려화%협민%정신생%한추%오이병
脑缺血%再灌注损伤%肿瘤坏死因子α%脑水肿%大鼠
腦缺血%再灌註損傷%腫瘤壞死因子α%腦水腫%大鼠
뇌결혈%재관주손상%종류배사인자α%뇌수종%대서
brain ischemia%reperfusion injury%tumor necrosis factor-α%brain edema%rats
目的 探讨脑缺血再灌注后缺血脑组织肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)与脑梗死组织水肿的关系.方法 SD大鼠随机分为脑缺血再灌注组(n=44)和假手术组(n=40).应用线栓法制备大鼠大脑中动脉闭塞2 h后再灌注模型,分别在再灌注后6 h、24 h、3 d、7 d通过2,3,5-三苯基氯化四氮唑染色法确定梗死灶大小,采用干、湿重法检测脑组织水含量评价脑水肿程度,以酶联免疫吸附法测定缺血脑组织TNF-α含量.结果 缺血脑组织TNF-α含量在再灌注6 h即升高,为(445.8±91.7)pg/ml,3 d达高峰,为(715.5±121.3)pg/ml,与假手术组和其他时间点比较均有显著差异(P均<0.001),此后逐渐下降,7 d时仍显著高于假手术组[(478.1±145.5)pg/ml对(148.5±101.7)pg/ml,P<0.005];脑组织水含量的起始变化滞后于TNF-α含量的增高,脑缺血再灌注24 h才显著增高(P<0.001),3 d达高峰(P<0.001),7 d时仍高于对照组(P<0.05);脑梗死体积演变与TNF-α水平变化一致.结论 TNF-α与大鼠脑缺血再灌注后脑水肿和梗死体积变化有关,对脑组织有损害作用.
目的 探討腦缺血再灌註後缺血腦組織腫瘤壞死因子-α(tumor necrosis factor-α,TNF-α)與腦梗死組織水腫的關繫.方法 SD大鼠隨機分為腦缺血再灌註組(n=44)和假手術組(n=40).應用線栓法製備大鼠大腦中動脈閉塞2 h後再灌註模型,分彆在再灌註後6 h、24 h、3 d、7 d通過2,3,5-三苯基氯化四氮唑染色法確定梗死竈大小,採用榦、濕重法檢測腦組織水含量評價腦水腫程度,以酶聯免疫吸附法測定缺血腦組織TNF-α含量.結果 缺血腦組織TNF-α含量在再灌註6 h即升高,為(445.8±91.7)pg/ml,3 d達高峰,為(715.5±121.3)pg/ml,與假手術組和其他時間點比較均有顯著差異(P均<0.001),此後逐漸下降,7 d時仍顯著高于假手術組[(478.1±145.5)pg/ml對(148.5±101.7)pg/ml,P<0.005];腦組織水含量的起始變化滯後于TNF-α含量的增高,腦缺血再灌註24 h纔顯著增高(P<0.001),3 d達高峰(P<0.001),7 d時仍高于對照組(P<0.05);腦梗死體積縯變與TNF-α水平變化一緻.結論 TNF-α與大鼠腦缺血再灌註後腦水腫和梗死體積變化有關,對腦組織有損害作用.
목적 탐토뇌결혈재관주후결혈뇌조직종류배사인자-α(tumor necrosis factor-α,TNF-α)여뇌경사조직수종적관계.방법 SD대서수궤분위뇌결혈재관주조(n=44)화가수술조(n=40).응용선전법제비대서대뇌중동맥폐새2 h후재관주모형,분별재재관주후6 h、24 h、3 d、7 d통과2,3,5-삼분기록화사담서염색법학정경사조대소,채용간、습중법검측뇌조직수함량평개뇌수종정도,이매련면역흡부법측정결혈뇌조직TNF-α함량.결과 결혈뇌조직TNF-α함량재재관주6 h즉승고,위(445.8±91.7)pg/ml,3 d체고봉,위(715.5±121.3)pg/ml,여가수술조화기타시간점비교균유현저차이(P균<0.001),차후축점하강,7 d시잉현저고우가수술조[(478.1±145.5)pg/ml대(148.5±101.7)pg/ml,P<0.005];뇌조직수함량적기시변화체후우TNF-α함량적증고,뇌결혈재관주24 h재현저증고(P<0.001),3 d체고봉(P<0.001),7 d시잉고우대조조(P<0.05);뇌경사체적연변여TNF-α수평변화일치.결론 TNF-α여대서뇌결혈재관주후뇌수종화경사체적변화유관,대뇌조직유손해작용.
Objective To investigate the relationship between tumor necrosis factor-α (TNF-α) in ischemic brain tissue and bran edema after cerebral ischemia-reperfusion in rats.Methods Eighty four male SD rats were randomly assigned to either a cerebral ischemia reperfusion group (n =44) or a sham-operation group (n =40). A model of middle cerebral artery occlusion for 120 minutes followed by reperfusion was induced in rats using the suture method. The infarct size was determined by 2, 3, 5-triphenyi terazoloride (TTC) staining at 6 h,24 h, 3 d, and 7 d respectively after the reperfusion. Dry-wet weight method was used to measure brain water content and evaluate the extent of brain edema. The enzyme-linked immunosorbent assay (ELISA) was used to detect the concentration of TNF-α in ischemic brain tissue. Results TNF-α level in ischemic brain tissue was increased at 6 h (445.8 ±91.7 pg/ml) after the reperfusion, and reached the peak at day 3 (715.5 ±121.3 pg/ml). There were significant differences compared to the sham-operation group and other time points (all P<0.001). After that, it was decreased gradually, but it was still higher than that in the shamoperation group at day 7 (478.1 ± 145.5 pg/ml vs. 148.5 ± 101.7 pg/ml, P<0.005). The initial change of the water content in brain tissue lagged behind the increased TNF-α. It did not increase significantly until 24 h after cerebral ischemia-reperfusion (P <0.001). It reached the peak at day 3 (P <0.001), and it was still higher than that in the control group at day 7 (P <0.05). The evolution of cerebral infarct volume was in accordance with the changes of TNF-α level. Conclusions TNF-α is associated with the changes of brain edema and infarct volume,and it is harmful to brain tissue.