摘要
目的研究大鼠重症急性胰腺炎(SAP)合并脑损伤时脑组织海马区核因子-κB p65(NF-κB p65)和半胱天冬氨酸蛋白酶3(Caspase-3)的表达及与脑损伤的关系。方法 4%牛磺胆酸钠逆行注入大鼠胰胆管建立SAP模型(SD大鼠32只,SAP组),对照组32只SD大鼠应用生理盐水(NS组)。尼氏染色检测脑组织海马区神经元损伤情况,免疫组化检测海马组织NF-κB p65和Caspase-3的蛋白表达。结果与NS组比较,在3、6、12h,SAP组NF-κB p65和Caspase-3的表达均明显增加,6h达高峰(P<0.05),且海马神经元损伤也明显加重(P<0.05)。结论 NF-κB p65参与了SAP大鼠脑损伤的发生、发展;NF-κB p65可能通过促进Caspase-3的表达来加速神经元凋亡。
[Abstract] Objective To investigate the relationship of the expressions of hyppocampal nuclear factor kappa 13 p65（NF-kB p65） and Caspase-3 in rats with brain injury in rats with severe acute pancreatitis（SAP）. Methods The SAP rat model was induced by retrograde injection of 4% sodium taurocholate into the bile-pancreatic duct in 32 SD rats （group A）. Another 32 rats were injected normal saline as the controls（group B）. Nissle stain was used to detect the severity of the brain injury. The expressions of NF-kB p65 and caspase-3 were detected by immunohistochemistry. Results Compared to group B, the expressions of NF-kB p65 and caspase-3 in group A were obviously increased at 3, 6 and 12 h,which peaked at 6 h（P〈0. 05）. The nuronal injury was more severe in group A than that in group B at 3,6 and 12 h,which peaked at 12 h（P〈0. 05）. Conclusion The brain injury in SAP rats showed high correlation with neuronal apoptosis in the early metaphase. NF-kB p65 is invulved in the occurrence and development of brain injury in rats with SAP, which probably accelerates the neuronal apoptosis through enhancing the expression of Caspase-3.
出处
《江苏医药》
CAS
CSCD
北大核心
2012年第17期2015-2017,F0002,共4页
Jiangsu Medical Journal
基金
南通大学自然科学项目(10Z058)
作者简介
通讯作者 黄中伟E-mail：doctorhzw@yahoo．com．cn
