中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2012年
5期
559-562
,共4页
周军%刘克玄%魏继承%王晓斌%唐显玲%黄文起
週軍%劉剋玄%魏繼承%王曉斌%唐顯玲%黃文起
주군%류극현%위계승%왕효빈%당현령%황문기
肠%再灌注损伤%小神经胶质细胞%脑
腸%再灌註損傷%小神經膠質細胞%腦
장%재관주손상%소신경효질세포%뇌
Intestines%Reperfusion injury%Microglia%Brain
目的 探讨肠缺血再灌注对大鼠脑组织小胶质细胞活化的影响.方法 清洁级健康成年雄性SD大鼠128只,体重250-300 g,采用随机数字表法,将其随机分为2组(n=64):假手术组(S组)和肠缺血再灌注组(I/R组).I/R组采用夹闭肠系膜上动脉90 min后再灌注的方法制备肠缺血再灌注损伤模型.于再灌注2、6、24、48 h时观察肠粘膜病理学结果,并行Chiu评分;取脑组织,计数活化的小胶质细胞,计算小胶质细胞活化率,测定脑组织活性氧(ROS)、MDA含量及SOD活性、NO含量、一氧化氮合酶(NOS)及诱导型一氧化氮合酶(iNOS)活性.结果 与S组比较,I/R组肠组织Chiu评分、脑组织活化的小胶质细胞数、小胶质细胞活化率、ROS、NOS和iNOS活性、MDA和NO含量升高,SOD活性降低(P<0.05或0.01);I/R组再灌注6-48 h脑组织ROS、NOS和iNOS活性、MDA和NO含量依次升高,脑组织SOD活性及肠组织Chiu评分依次降低,脑组织活化的小胶质细胞和小胶质细胞活化率于再灌注24h时达峰值(P<0.05或0.01).结论 肠缺血再灌注可通过激活脑组织小胶质细胞,激活NOS和促进ROS生成,从而诱发脂质过氧化反应,该作用作为肠缺血再灌注诱发大鼠脑损伤的机制.
目的 探討腸缺血再灌註對大鼠腦組織小膠質細胞活化的影響.方法 清潔級健康成年雄性SD大鼠128隻,體重250-300 g,採用隨機數字錶法,將其隨機分為2組(n=64):假手術組(S組)和腸缺血再灌註組(I/R組).I/R組採用夾閉腸繫膜上動脈90 min後再灌註的方法製備腸缺血再灌註損傷模型.于再灌註2、6、24、48 h時觀察腸粘膜病理學結果,併行Chiu評分;取腦組織,計數活化的小膠質細胞,計算小膠質細胞活化率,測定腦組織活性氧(ROS)、MDA含量及SOD活性、NO含量、一氧化氮閤酶(NOS)及誘導型一氧化氮閤酶(iNOS)活性.結果 與S組比較,I/R組腸組織Chiu評分、腦組織活化的小膠質細胞數、小膠質細胞活化率、ROS、NOS和iNOS活性、MDA和NO含量升高,SOD活性降低(P<0.05或0.01);I/R組再灌註6-48 h腦組織ROS、NOS和iNOS活性、MDA和NO含量依次升高,腦組織SOD活性及腸組織Chiu評分依次降低,腦組織活化的小膠質細胞和小膠質細胞活化率于再灌註24h時達峰值(P<0.05或0.01).結論 腸缺血再灌註可通過激活腦組織小膠質細胞,激活NOS和促進ROS生成,從而誘髮脂質過氧化反應,該作用作為腸缺血再灌註誘髮大鼠腦損傷的機製.
목적 탐토장결혈재관주대대서뇌조직소효질세포활화적영향.방법 청길급건강성년웅성SD대서128지,체중250-300 g,채용수궤수자표법,장기수궤분위2조(n=64):가수술조(S조)화장결혈재관주조(I/R조).I/R조채용협폐장계막상동맥90 min후재관주적방법제비장결혈재관주손상모형.우재관주2、6、24、48 h시관찰장점막병이학결과,병행Chiu평분;취뇌조직,계수활화적소효질세포,계산소효질세포활화솔,측정뇌조직활성양(ROS)、MDA함량급SOD활성、NO함량、일양화담합매(NOS)급유도형일양화담합매(iNOS)활성.결과 여S조비교,I/R조장조직Chiu평분、뇌조직활화적소효질세포수、소효질세포활화솔、ROS、NOS화iNOS활성、MDA화NO함량승고,SOD활성강저(P<0.05혹0.01);I/R조재관주6-48 h뇌조직ROS、NOS화iNOS활성、MDA화NO함량의차승고,뇌조직SOD활성급장조직Chiu평분의차강저,뇌조직활화적소효질세포화소효질세포활화솔우재관주24h시체봉치(P<0.05혹0.01).결론 장결혈재관주가통과격활뇌조직소효질세포,격활NOS화촉진ROS생성,종이유발지질과양화반응,해작용작위장결혈재관주유발대서뇌손상적궤제.
Objective To investigate the effects of intestinal ischemia-reperfusion(I/R)on cerebral microglial activation in rats.Methods One hundred and twenty-eight healthy male SD rats weighing 250-300 g were randomly allocated to one of two groups(n =64 each):group sham operation(group S)and intestinal I/R group.Intestinal I/R was produced by occlusion of superior mesenteric stery for 90 main followed by reperfusion.Sixteen animals were sacrificed at each of the 4 time points:2,6,24 and 48 h of reperfusion in each group.Their intestines were obtained for microscopic examination.Their brains were harvested for detection of microglial activation (by immuno-histochemistry).The reactive oxygen species(ROS),MDA and NO contents and SOD,nitric oxide synthase(NOS)and inducible nitric oxide synthase(iNOS)activities in the brain were measured.Results The microglia were in quiescent condition.Ibal staining was negative or light in group S.Intestinal I/R significantly increased intestinal Chiu score,cerebral microglial activation at 6,24 and 48 h of repeffusion which peaked at 24 h of reperfusion in group I/R as compared with group S.Cerebral ROS,MDA,NO levels and NOS,iNOS activities were significantly higher while SOD activity was significantly lower in group I/R than in group S.Concluslon Intestinal I/R can activate microglia and induce the release of nitrogen and oxygen free radicals resulting in cerebral injury.