CAJ | 학술논문

目的评价肠缺血再灌注对大鼠脑的影响.方法健康雄性成年SD大鼠64只,采用随机数字表法,将其随机分为2组(n=32):假手术组(S组)和肠缺血再灌注组(II/R组),采用Morris水迷宫实验测定认知功能,随后II/R组采用夹闭肠系膜上动脉90min后再灌注的方法制备肠缺血再灌注模型,S组仅分离肠系膜上动脉,不夹闭.于再灌注2、6、12、24 h时各组随机取8只大鼠,经心脏取血2ml后,取肠及脑组织,光镜下观察病理学结果,采用改良Chiu评分法评价肠粘膜损伤程度,采用ELISA法测定血浆TNF-α和IL-6浓度,采用TUNEL法检测皮层脑组织细胞凋亡情况;于再灌注24 h时采用Morris水迷宫实验测试认知功能.结果 S组大鼠肠及脑组织镜下结构未见异常,II/R组再灌注6 h后可见明显肠道和脑损伤.与S组比较,II/R组再灌注2、6、12和24 h时Chiu评分、血浆TNF-α及IL-6浓度升高,再灌注6、12和24 h时细胞凋亡数增加,再灌注24 h时大鼠潜伏期、游泳距离增加,穿越平台次数减少(P＜0.05或0.01),游泳速度差异无统计学意义(P＞0.05).结论肠缺血再灌注损伤可诱发大鼠脑损伤,引起认知功能减退,可能与炎性介质的释放及神经细胞凋亡有关.
목적 평개장결혈재관주대대서뇌적영향.방법 건강웅성성년SD대서64지,채용수궤수자표법,장기수궤분위2조(n=32):가수술조(S조)화장결혈재관주조(II/R조),채용Morris수미궁실험측정인지공능,수후II/R조채용협폐장계막상동맥90min후재관주적방법제비장결혈재관주모형,S조부분리장계막상동맥,불협폐.우재관주2、6、12、24 h시각조수궤취8지대서,경심장취혈2ml후,취장급뇌조직,광경하관찰병이학결과,채용개량Chiu평분법평개장점막손상정도,채용ELISA법측정혈장TNF-α화IL-6농도,채용TUNEL법검측피층뇌조직세포조망정황;우재관주24 h시채용Morris수미궁실험측시인지공능.결과 S조대서장급뇌조직경하결구미견이상,II/R조재관주6 h후가견명현장도화뇌손상.여S조비교,II/R조재관주2、6、12화24 h시Chiu평분、혈장TNF-α급IL-6농도승고,재관주6、12화24 h시세포조망수증가,재관주24 h시대서잠복기、유영거리증가,천월평태차수감소(P＜0.05혹0.01),유영속도차이무통계학의의(P＞0.05).결론 장결혈재관주손상가유발대서뇌손상,인기인지공능감퇴,가능여염성개질적석방급신경세포조망유관.
Objective To investigate the effects of intestinal ischemia-reperfusion (I/R) on the brain in rats. Methods Sixty-four healthy male SD rats weighing 250-300 g were randomly allocated to one of 2 groups (n = 32 each): sham operation group (S) and intestinal I/R group (I/R). Intestinal I/R was produced by occlusion of superior mesenteric artery (SMA) for 90 min followed by reperfusion. Eight animals were sacrificed at each of the following time points: 2, 6, 12 and 24 h of reperfusion (T1-4) in each group. After a median sternotomyblood samples were taken from left ventricle for measurement of plasma TNF-α and IL-6 (by ELISA). Intestine and brain tissue was harvested for microscopic examination and detection of apoptosis ( by TUNEL). The cognitive function was tested using Morris water maze at 24 h. Results No abnormality was found in intestine and brain tissue in group S. Intestinal damage and neurodegeneration were detected in group I/R. Intestinal I/R significantly increased cerebral apoptosis in group I/R compared with group S. Plasma TNF-a and IL-6 concentrations were significantly higher at T1-4 in group I/R than in group S. The escape latency and swimming distance were significantly increased, while the number of crossing the platform was decreased in group I/R compared with group S. There was no significant difference in the swimming speed between the 2 groups. Conclusion Intestinal I/R can induce brain injury and lead to cognitive dysfunction. I/R-induced release of inflammatory mediators and neuronal apoptosis are involved in the underlying mechanism.