中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2010年
1期
86-90
,共5页
王胜军%迟兆富%王树华%迟令懿%赵秀鹤
王勝軍%遲兆富%王樹華%遲令懿%趙秀鶴
왕성군%지조부%왕수화%지령의%조수학
癫痫%聚腺苷二磷酸核糖聚合酶%NF-κB%白细胞介素1%环氧化酶-2
癲癇%聚腺苷二燐痠覈糖聚閤酶%NF-κB%白細胞介素1%環氧化酶-2
전간%취선감이린산핵당취합매%NF-κB%백세포개소1%배양화매-2
Epilepsy%Poly adenosine diphosphate-ribose polymerase%NF-kappa B%Interleukin-1%Cyclooxygenase-2
目的: 探讨癫痫大鼠海马组织核转录因子κB(NF-κB)随时间的变化规律及聚腺苷二磷酸核糖聚合酶(PARP)抑制剂3-氨基苯甲酰胺(3-AB)对NF-κB及白细胞介素1β(IL-1β)、环氧化酶-2(COX-2)的调节作用.方法: 应用Western blotting检测海藻氨酸致痫大鼠海马核蛋白中NF-κB p65在不同时点及3-AB干预癫痫大鼠后的表达;应用RT-PCR及Western blotting检测IL-1β、COX-2 mRNA和蛋白水平在3-AB干预前后的变化.结果: 大鼠海马核蛋白内NF-κB p65在癫痫后2 h开始增高(P<0.05),持续12 h(P<0.05),24 h后恢复至对照组水平;应用3-AB后,NF-κB p65在核蛋白中含量明显下降(P<0.05);癫痫发作6 h海马组织内IL-1β、COX-2 mRNA和蛋白水平表达增高(P<0.05),3-AB干预显著降低IL-1β、COX-2 mRNA及蛋白的表达(P<0.05).结论: 癫痫发作可诱发海马组织NF-κB的核转位及 IL-1β、COX-2的表达,3-AB能明显抑制癫痫诱发的NF-κB核转位及IL-1β、COX-2的表达.
目的: 探討癲癇大鼠海馬組織覈轉錄因子κB(NF-κB)隨時間的變化規律及聚腺苷二燐痠覈糖聚閤酶(PARP)抑製劑3-氨基苯甲酰胺(3-AB)對NF-κB及白細胞介素1β(IL-1β)、環氧化酶-2(COX-2)的調節作用.方法: 應用Western blotting檢測海藻氨痠緻癇大鼠海馬覈蛋白中NF-κB p65在不同時點及3-AB榦預癲癇大鼠後的錶達;應用RT-PCR及Western blotting檢測IL-1β、COX-2 mRNA和蛋白水平在3-AB榦預前後的變化.結果: 大鼠海馬覈蛋白內NF-κB p65在癲癇後2 h開始增高(P<0.05),持續12 h(P<0.05),24 h後恢複至對照組水平;應用3-AB後,NF-κB p65在覈蛋白中含量明顯下降(P<0.05);癲癇髮作6 h海馬組織內IL-1β、COX-2 mRNA和蛋白水平錶達增高(P<0.05),3-AB榦預顯著降低IL-1β、COX-2 mRNA及蛋白的錶達(P<0.05).結論: 癲癇髮作可誘髮海馬組織NF-κB的覈轉位及 IL-1β、COX-2的錶達,3-AB能明顯抑製癲癇誘髮的NF-κB覈轉位及IL-1β、COX-2的錶達.
목적: 탐토전간대서해마조직핵전록인자κB(NF-κB)수시간적변화규률급취선감이린산핵당취합매(PARP)억제제3-안기분갑선알(3-AB)대NF-κB급백세포개소1β(IL-1β)、배양화매-2(COX-2)적조절작용.방법: 응용Western blotting검측해조안산치간대서해마핵단백중NF-κB p65재불동시점급3-AB간예전간대서후적표체;응용RT-PCR급Western blotting검측IL-1β、COX-2 mRNA화단백수평재3-AB간예전후적변화.결과: 대서해마핵단백내NF-κB p65재전간후2 h개시증고(P<0.05),지속12 h(P<0.05),24 h후회복지대조조수평;응용3-AB후,NF-κB p65재핵단백중함량명현하강(P<0.05);전간발작6 h해마조직내IL-1β、COX-2 mRNA화단백수평표체증고(P<0.05),3-AB간예현저강저IL-1β、COX-2 mRNA급단백적표체(P<0.05).결론: 전간발작가유발해마조직NF-κB적핵전위급 IL-1β、COX-2적표체,3-AB능명현억제전간유발적NF-κB핵전위급IL-1β、COX-2적표체.
AIM:To investigate the time course of nuclear factor-κB (NF-κB) and the effects of 3-aminobenzamide (3-AB) on the expressions of NF-κB,interleukin-1β (IL-1β) and cyclooxygenase-2 (COX-2) in hippocampus after seizures. METHODS:Epilepsy were induced by kainic acid through cerebral ventricular injection. Western blotting was used to detect NF-κB p65 expression in nucleus at various experiment groups. Moreover,mRNA and protein expressions of IL-1β and COX-2 in different experiment groups were determined by RT-PCR and Western blotting analysis. RESULTS:NF-κB p65 immunoreactivity began to increase in the nuclear fraction at 2 h (P<0.05),kept rising at 12 h (P<0.05) and returned to control level at 24 h after epilepsy seizures. Furthermore,3-AB sharply decreased the accumulation of NF-κB p65 in nucleus (P<0.05). In addition,3-AB significantly decreased the mRNA and protein expressions of IL-1β and COX-2 which obviously increased in hippocampus at 6 h after epilepsy seizures (P<0.05). CONCLUSION:Seizures triggers NF-κB nucleus translocation and promotes the expressions of IL-1β and COX-2 in hippocampus. In addition,poly (adenosine diphosphate-ribose) polymerase inhibition by 3-AB suppresses NF-κB associated inflammatory pathway in epileptic rat hippocampus.
