CAJ | 학술논문

目的观察芹菜素对局灶性脑缺血再灌注大鼠神经功能的影响,并探讨其相关作用机制.方法将90只大鼠随机分为假手术组、模型组及芹菜素组.采用线栓法将模型组和芹菜素组大鼠制成左侧大脑中动脉缺血再灌注(1.5 h)模型,假手术组大鼠在制模过程中不阻断大脑中动脉血流.芹菜索组大鼠于再灌注同时及其后每24 h腹腔注射芹菜素液,假手术组及模型组大鼠则在相同时间点注射等体积生理盐水.于再灌注第24,48,72小时及第7天时参照Zea longa法评定大鼠神经功能缺损程度,同时采用光镜、电镜观察各组大鼠脑组织病理形态学改变,选用ELISA法测定脑组织肿瘤坏死因子-α(TNF-αβ)和白细胞介素-1β(1L-1β)含量.结果模型组大鼠神经功能缺损症状于脑缺血再灌注第7天时明显改善,芹菜素组大鼠神经功能缺损症状于脑缺血再灌注第72小时时即有显著提高.与假手术组比较,模型组、芹菜素组TNF-α和IL-1β含量均显著增高(P<0.01),芹菜素组TNF-α、IL-1β含量在脑缺血再灌注第48和72小时时均较模型组显著降低(P<0.05).进一步分析后发现,大鼠神经功能缺损评分均与IL-1β含量、TNF-α含量呈正相关.模型组大鼠脑皮质和海马细胞肿胀、细胞间质水肿,有空泡形成,神经细胞均有核同缩、碎裂、溶解表现.芹菜素组大鼠脑组织神经细胞轻度肿胀,细胞间质、毛细血管壁轻微水肿,神经细胞有明显核固缩、碎裂、溶解表现.结论芹菜素能促进局部脑缺血冉灌注大鼠神经功能恢复,其作用机制町能与下调TNF-α和IL-1β水平有关.
목적 관찰근채소대국조성뇌결혈재관주대서신경공능적영향,병탐토기상관작용궤제.방법 장90지대서수궤분위가수술조、모형조급근채소조.채용선전법장모형조화근채소조대서제성좌측대뇌중동맥결혈재관주(1.5 h)모형,가수술조대서재제모과정중불조단대뇌중동맥혈류.근채색조대서우재관주동시급기후매24 h복강주사근채소액,가수술조급모형조대서칙재상동시간점주사등체적생리염수.우재관주제24,48,72소시급제7천시삼조Zea longa법평정대서신경공능결손정도,동시채용광경、전경관찰각조대서뇌조직병리형태학개변,선용ELISA법측정뇌조직종류배사인자-α(TNF-αβ)화백세포개소-1β(1L-1β)함량.결과 모형조대서신경공능결손증상우뇌결혈재관주제7천시명현개선,근채소조대서신경공능결손증상우뇌결혈재관주제72소시시즉유현저제고.여가수술조비교,모형조、근채소조TNF-α화IL-1β함량균현저증고(P<0.01),근채소조TNF-α、IL-1β함량재뇌결혈재관주제48화72소시시균교모형조현저강저(P<0.05).진일보분석후발현,대서신경공능결손평분균여IL-1β함량、TNF-α함량정정상관.모형조대서뇌피질화해마세포종창、세포간질수종,유공포형성,신경세포균유핵동축、쇄렬、용해표현.근채소조대서뇌조직신경세포경도종창,세포간질、모세혈관벽경미수종,신경세포유명현핵고축、쇄렬、용해표현.결론 근채소능촉진국부뇌결혈염관주대서신경공능회복,기작용궤제정능여하조TNF-α화IL-1β수평유관.
Objective To observe the effect of apigenin on the recovery of neurological function following cerebral ischemia-reperfusion and investigate its mechanism. Methods Ninety male Sprague-Dawley rats were randomized into a sham-operated group, a model group and an apigenin-treated group. A transient ( 1.5 h) focal cerebral ischemia-reperfu-sion model was established in the rats of the model and apigenin-treated groups. In the sham-operated rats the middle cere-bral artery was not occluded. The rats in the apigenin-treated group received an intra-abdominal injection of apigenin, and the rats in the other two groups received injections of normal saline solution. Neurological behavior scores were assessed in accordance with the Zea Longa method at the 24th, 48th and 72nd hour and the 7th day after reperfusion. Cellular and sub-cellular morphology were observed with an optical microscope and an electron microscope, and the levels of TNF-α and IL-1β were measured using ELISA. Results Neurological function improved by the 7th day after reperfusion in the model group, but improved significantly by the 72nd hour after reperfusion in the apigenin-treated group. Average TNF-α and IL-1β levels in the model group and the apigenin-treated group were significantly higher than in the sham-operated group. Av-erage TNF-α and IL-1β levels in the apigenin-treated group were significantly lower than in the model group at the 48th and 72nd hour after reperfusion. Neurological behavior scores had a positive correlation with the IL-1β and TNF-α levels. In the model group, obvious intracellular and intercellular edema and vacuolization were observed in the ischemic cortices and hippocampuses, with remarkable karyopycnosis and organelle broadening and dissolution and vacuolization in glial cells and neurons. In the apigenin-treated group, similar but significantly milder morphological changes were observed. Conclusion Apigenin can promote the recovery of neurological function in rats by downregulating the expression of TNF-α and IL-1βfollowing focal cerebral ischemia-reperfusion.