河北医药
河北醫藥
하북의약
HEBEI MEDICAL JOURNAL
2014年
6期
812-815
,共4页
王恒%邵恩得%张金荣%吴立华
王恆%邵恩得%張金榮%吳立華
왕항%소은득%장금영%오립화
核因子-κB%脑出血%胆囊收缩素-8%炎症
覈因子-κB%腦齣血%膽囊收縮素-8%炎癥
핵인자-κB%뇌출혈%담낭수축소-8%염증
NF-κB%cerebral hemorrhage%CCK-8%inflammation
目的:探讨胆囊收缩素-8(cholecystokinin-8,CCK-8)对高血压性大鼠脑出血后血肿周围组织核因子-κB ( Necular Factor Kappa B ,NF-κB)活性的影响。方法取成年SD大鼠72只,体重250~300 g,随机分假手术组( n =12)、脑出血组( n =24)和CCK-8治疗组( n =24)。采用电泳迁移率改变分析方法(electrophoretic mobility shift assay , EMSA)检测核内NF-κB的活性,用免疫组化方法观察NF-κB在细胞内的表达情况,并用干湿重法测量出血侧脑组织含水量。结果脑出血组各时间点NF-κB的活性以及脑含水量较假手术组和CCK-8治疗均有明显增高( P <0妹.05)。结论脑出血后,脑组织NF-κB的表达明显增加,CCK-8可以有效的抑制NF-κB的活性,这对于减轻NF-κB在脑出血后介导的继发性炎性损害起到了积极的作用。
目的:探討膽囊收縮素-8(cholecystokinin-8,CCK-8)對高血壓性大鼠腦齣血後血腫週圍組織覈因子-κB ( Necular Factor Kappa B ,NF-κB)活性的影響。方法取成年SD大鼠72隻,體重250~300 g,隨機分假手術組( n =12)、腦齣血組( n =24)和CCK-8治療組( n =24)。採用電泳遷移率改變分析方法(electrophoretic mobility shift assay , EMSA)檢測覈內NF-κB的活性,用免疫組化方法觀察NF-κB在細胞內的錶達情況,併用榦濕重法測量齣血側腦組織含水量。結果腦齣血組各時間點NF-κB的活性以及腦含水量較假手術組和CCK-8治療均有明顯增高( P <0妹.05)。結論腦齣血後,腦組織NF-κB的錶達明顯增加,CCK-8可以有效的抑製NF-κB的活性,這對于減輕NF-κB在腦齣血後介導的繼髮性炎性損害起到瞭積極的作用。
목적:탐토담낭수축소-8(cholecystokinin-8,CCK-8)대고혈압성대서뇌출혈후혈종주위조직핵인자-κB ( Necular Factor Kappa B ,NF-κB)활성적영향。방법취성년SD대서72지,체중250~300 g,수궤분가수술조( n =12)、뇌출혈조( n =24)화CCK-8치료조( n =24)。채용전영천이솔개변분석방법(electrophoretic mobility shift assay , EMSA)검측핵내NF-κB적활성,용면역조화방법관찰NF-κB재세포내적표체정황,병용간습중법측량출혈측뇌조직함수량。결과뇌출혈조각시간점NF-κB적활성이급뇌함수량교가수술조화CCK-8치료균유명현증고( P <0매.05)。결론뇌출혈후,뇌조직NF-κB적표체명현증가,CCK-8가이유효적억제NF-κB적활성,저대우감경NF-κB재뇌출혈후개도적계발성염성손해기도료적겁적작용。
Objective To investigate the effect of cholecystokinin-8 ( CCK-8 ) on the changes of Necular Factor Kappa B ( NF-κB) activity in rats with hypertensive intracerebral hemorrhage .Methods Seventy-two adult Sprague-Dawley rats,weighted 250 ~300 g, were randomly divided into three groups: control group , cerebral hemorrhage group and CCK-8 treatment group.The activity of NF-κB was detected by electrophoretic mobility shift assay ( EMSA) and the expression of NF-κB in cells was detected by immunohistochemical methods ,and water content in brain tissue of injury part was measured . Results The activity of NF-κB and brain water content in cerebral hemorrhage group were significantly increased , as compared with those in control group and CCK-8 group ( P <0.05).Conclusion The expression levels of NF-κB are obviously increased immediately after intracerebral hemorrhage ,and CCK-8 can inhibit effectively the activity of NF-κB,which relieves the damage of secondary inflammatory reaction induced by NF-κB after intracerebral hemorrhage .