中华胰腺病杂志
中華胰腺病雜誌
중화이선병잡지
CHINESE JOURNAL OF PANCREATOLOGY
2011年
2期
120-122
,共3页
袁伟燕%周国雄%黄华%许海玲%黄中伟
袁偉燕%週國雄%黃華%許海玲%黃中偉
원위연%주국웅%황화%허해령%황중위
胰腺炎,急性坏死性%脑损伤%神经元%细胞凋亡%核转录因子-κB
胰腺炎,急性壞死性%腦損傷%神經元%細胞凋亡%覈轉錄因子-κB
이선염,급성배사성%뇌손상%신경원%세포조망%핵전록인자-κB
Pancreatitis,acute necrotizing%Brain injury%Neurons%Apoptosis%Nuclear factor-κB
目的 探讨急性坏死性胰腺炎(ANP)大鼠合并脑损伤时脑组织海马神经元凋亡及其与NF-κB p65之间的关系.方法 64只SD大鼠按数字表法随机分为生理盐水(NS)组和ANP组.胰胆管逆行注入4%牛磺胆酸钠制备ANP模型.尼氏染色法检测脑组织海马神经元的损伤,TUNEL法检测神经元凋亡,RT-PCR法及免疫组化法检测海马组织NF-κB p65 mRNA和蛋白的表达.结果 ANP组大鼠海马神经元缺失,胞核固缩,核仁欠清晰,尼氏小体减少或消失,损伤随时间延长逐渐加重.ANP组大鼠制模后3、6、12 h的神经元凋亡指数分别为10.63±0.24、21.02±0.25、17.12±0.36,显著高于NS组同时点的0.33±0.19、0.71±0.67、0.45±0.33(P值均＜0.01);NF-κB p65 mRNA表达量分别为0.63±0.05、1.05±0.06、0.92±0.05,显著高于NS组同时点的0.11±0.01、0.12±0.01、0.08±0.01(P值均＜0.05).NF-κB p65蛋白的变化与其mRNA的变化一致.结论 ANP大鼠脑损伤的早、中期与神经元凋亡关系密切,其机制可能与NF-κB p65的激活有关.
目的 探討急性壞死性胰腺炎(ANP)大鼠閤併腦損傷時腦組織海馬神經元凋亡及其與NF-κB p65之間的關繫.方法 64隻SD大鼠按數字錶法隨機分為生理鹽水(NS)組和ANP組.胰膽管逆行註入4%牛磺膽痠鈉製備ANP模型.尼氏染色法檢測腦組織海馬神經元的損傷,TUNEL法檢測神經元凋亡,RT-PCR法及免疫組化法檢測海馬組織NF-κB p65 mRNA和蛋白的錶達.結果 ANP組大鼠海馬神經元缺失,胞覈固縮,覈仁欠清晰,尼氏小體減少或消失,損傷隨時間延長逐漸加重.ANP組大鼠製模後3、6、12 h的神經元凋亡指數分彆為10.63±0.24、21.02±0.25、17.12±0.36,顯著高于NS組同時點的0.33±0.19、0.71±0.67、0.45±0.33(P值均＜0.01);NF-κB p65 mRNA錶達量分彆為0.63±0.05、1.05±0.06、0.92±0.05,顯著高于NS組同時點的0.11±0.01、0.12±0.01、0.08±0.01(P值均＜0.05).NF-κB p65蛋白的變化與其mRNA的變化一緻.結論 ANP大鼠腦損傷的早、中期與神經元凋亡關繫密切,其機製可能與NF-κB p65的激活有關.
목적 탐토급성배사성이선염(ANP)대서합병뇌손상시뇌조직해마신경원조망급기여NF-κB p65지간적관계.방법 64지SD대서안수자표법수궤분위생리염수(NS)조화ANP조.이담관역행주입4%우광담산납제비ANP모형.니씨염색법검측뇌조직해마신경원적손상,TUNEL법검측신경원조망,RT-PCR법급면역조화법검측해마조직NF-κB p65 mRNA화단백적표체.결과 ANP조대서해마신경원결실,포핵고축,핵인흠청석,니씨소체감소혹소실,손상수시간연장축점가중.ANP조대서제모후3、6、12 h적신경원조망지수분별위10.63±0.24、21.02±0.25、17.12±0.36,현저고우NS조동시점적0.33±0.19、0.71±0.67、0.45±0.33(P치균＜0.01);NF-κB p65 mRNA표체량분별위0.63±0.05、1.05±0.06、0.92±0.05,현저고우NS조동시점적0.11±0.01、0.12±0.01、0.08±0.01(P치균＜0.05).NF-κB p65단백적변화여기mRNA적변화일치.결론 ANP대서뇌손상적조、중기여신경원조망관계밀절,기궤제가능여NF-κB p65적격활유관.
Objective To investigate the relationship between expression of nuclear factor kappa B p65 ( NF-κB p65) and hippocampal neuronal apoptosis in acute necrotizing pancreatitis (ANP) rats with brain injury. Methods Sixty-four SD rats were randomized into normal saline group (NS) and ANP group. The ANP rat model was induced by retrograde injection of 4% sodium taurocholate into the pancreaticobiliary duct of SD rats. Nissle stain was used to detect the brain injury. Neuronal apoptosis was determined by TUNEL.NF-κB p65 expression was detected by immunohistochemistry and RT-PCR. Results Hippocampal neuron was absent, karyopyknosis, unclear nucleolus and decreased Nissl bodies were found, the injuries was aggravated with time. The apoptosis index at the 3, 6 and 12 h in ANP group was 10.63 ±0.24, 21.02±0.25, 17.12±0.36, respectively, while they were 0.33±0.19,0.71±0.67, 0.45 ± 0. 33 in NS group, and the difference was statistically significant ( P ＜ 0. 01 ). The expressions of NF-κB p65 mRNA were 0. 63 ± 0.05,1.05 ±0.06,0.92 ±0.05, which were significantly higher than those in the NS group (0.11 ±0.01,0.12±0.01,0.08±0.01,P＜0.05).The chatge of expression of NF±κB p65 protein was consistent with that of NF-κB p65 mRNA. Conclusions The brain injury of ANP rats was highly correlated with neuronal apoptosis at the early and middle phase of ANP, and its mechanism may be related with NF-κB p65 activation.
