姜黄素对急性肺栓塞大鼠核转录因子kappa B的影响

目的：探索姜黄素（CUR）对急性肺栓塞（APE）大鼠肺组织核转录因子kappa B（NF-κB）的影响。方法：72只SD大鼠随机分为4组,对照、假手术、模型和CUR治疗组。采用自体血栓复制法制备APE大鼠模型,栓塞后6h、24h和72h分别随机取各组大鼠各6只,水合氯醛麻醉后取肺组织病理检查,Western免疫印迹分析NF-κB蛋白的表达水平,免疫组化染色检测NF-κB阳性细胞数。结果：肺组织病理证实典型APE的血栓及肺泡坏死出血,CUR治疗能够减轻肺组织的病变。免疫组化染色可见在肺泡细胞、巨噬细胞、支气管上皮细胞及支气管平滑肌周围均有不同程度的NF-κB蛋白表达。栓塞后6 h、24 h和72 h,CUR治疗组的NF-κB阳性细胞计数明显低于模型组（P〈0.001）,接近对照和假手术组。栓塞后6 h、24 h时,Western免疫印迹显示CUR治疗组NF-κB蛋白的表达水平低于模型组（P〈0.01）,接近对照和假手术组。结论：CUR可通过下调APE大鼠肺组织NF-κB转录因子的表达水平而改善其肺部的损害,这可能是其干预APE的机制之一。

Effects of Curcumine on NF- kB in Acute Pulmonary Embolism Rats

Objective：To explore the effects of curcumine （CUR） on NF-kB in the lung tissues of acute puhnonary embolism （APE） rats. Methods ：72 SD rats were randomly divided into four groups ： control group, sham group, APE model group, curcumine group. Each APE model was established by autologous blood clot. At 6 h,24 h and 72 h after embolism, lung tissues were collected in 6 rats of each group for pathological examination to observe the changes in the lung organization and Western blot was used to analyze the expression of NF -kB and immunohistochemical staining was used to access amounts of NF-kB positive cells. Result ：Typical thrombus and alveolar hemorrhage necrosis were seen in the pathological examination of APE rats and CUR can relieve the damage. Immunohistochemical method result displayed that different lev- els of NF -kB were expressed in the alveolar cells, macrophages, bronchial epithelial cells and bronchial smooth muscle. The positive cells of NF -kB in CUR group was obviously lower than that of the model group at 6 h,24 h and 72 h after embolism （ P 〈 0.001 ） but were approach to that of the control and sham groups. According to Western blot result, the NF -kB protein level in the lung tissue in CUR group was lower than that in the model group at 6 h and 24 h （P 〈 0.01 ）but approach to that in the control and sham groups. Conclusion：Curcumine can lessen the damage to the lung in APE rats by suppressing the expressions of NF -kB and this could be one of the mechanisms for CUR to intervene APE rats.