CAJ | 학술논문

目的：观察慢性脑低灌注大鼠海马组织中干扰素-γ、TNF-α、诱导型 NO合酶（iNOS）、吲哚胺2，3-双加氧酶（IDO）和犬尿氨酸（KYN）的表达，探讨慢性脑低灌注致认知功能损害大鼠海马组织中KYN通路相关代谢产物的变化特点。方法选择Wistar大鼠30只，随机分为假手术组15只和双侧颈总动脉永久性结扎组（2VO组）15只。制作慢性脑低灌注大鼠模型，Morris水迷宫检测2VO大鼠空间学习与记忆能力变化，免疫组织化学检测大鼠海马CA1区iNOS、干扰素-γ和TNF-α的表达，ELISA法检测IDO及KYN的水平。结果与假手术组比较，2VO组大鼠第3天开始逃避潜伏期明显延长，平台象限游泳距离百分比明显减少，iNOS、干扰素-γ及TNF-α阳性表达，IDO和KYN水平明显升高[（4．73±0．21）ng/ml vs （0．89±0．06）ng/ml和（1．55±0．12）ng/ml vs （0．19±0．02） ng/ml ，P＜0．05]。结论慢性脑灌注大鼠的病理生理过程包含着炎性反应，而炎性反应的发生很可能刺激了IDO和KYN的高表达，KYN和IDO的蓄积有可能参与其导致认知障碍的过程。
목적：관찰만성뇌저관주대서해마조직중간우소-γ、TNF-α、유도형 NO합매（iNOS）、신타알2，3-쌍가양매（IDO）화견뇨안산（KYN）적표체，탐토만성뇌저관주치인지공능손해대서해마조직중KYN통로상관대사산물적변화특점。방법선택Wistar대서30지，수궤분위가수술조15지화쌍측경총동맥영구성결찰조（2VO조）15지。제작만성뇌저관주대서모형，Morris수미궁검측2VO대서공간학습여기억능력변화，면역조직화학검측대서해마CA1구iNOS、간우소-γ화TNF-α적표체，ELISA법검측IDO급KYN적수평。결과여가수술조비교，2VO조대서제3천개시도피잠복기명현연장，평태상한유영거리백분비명현감소，iNOS、간우소-γ급TNF-α양성표체，IDO화KYN수평명현승고[（4．73±0．21）ng/ml vs （0．89±0．06）ng/ml화（1．55±0．12）ng/ml vs （0．19±0．02） ng/ml ，P＜0．05]。결론만성뇌관주대서적병리생리과정포함착염성반응，이염성반응적발생흔가능자격료IDO화KYN적고표체，KYN화IDO적축적유가능삼여기도치인지장애적과정。
Objective To study the features of kynurenine (KYN )pathway metabolites in hippo-campus of rats with cognitive impairment induced by chronic cerebral hypoperfusion by observing the expressions of IFN-γ,TNF-α,iNOS ,IDO and KYN .Methods Thirty Wistar rats were ran-domly divided into sham operation group and bilateral carotid artery permanent ligation group (15 in each group) .A rat model of chronic cerebral hypoperfusion was established .Spatial learning and memory ability in bilateral carotid artery permanent ligation group was tested in Morris water maze .Expressions of iNOS ,IFN-γ ,TNFαin hippocampal CA1 area were detected by immunohisto-chemistry and ELISA ,respectively .Results The escape latency period was significantly longer while the platform quadrant swimming distance was significantly shorter in bilateral carotid artery permanent ligation group than in sham operation group (P<0 .05) .Immunohistochemical staining showed that the expression levels of iNOS ,INF-γ ,TNF-α,IDO and KYN were significantly high-er in bilateral carotid artery permanent ligation group than in sham operation group (P<0 .05) . Conclusion The pathophysiological process in rats with chronic cerebral perfusion includes in-flammatory response which may stimulate the over-expression of IDO and KYN .Accumulated KYN and IDO may be involved in cognitive impairment induced by chronic cerebral hypoperfusion .