姜黄素对急性肺栓塞大鼠核转录因子kappa B的影响

来源 :中华中医药学刊 | 被引量 : 0次 | 上传用户:conglishan
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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。 Objective: To explore the effect of curcumin (CUR) on nuclear factor kappa B (NF-κB) in lung tissue of rats with acute pulmonary embolism (APE). Methods: Seventy-two SD rats were randomly divided into 4 groups: control, sham operation, model and CUR treatment group. APE rat model was established by autologous thrombus replication method. Six rats in each group were randomly selected at 6h, 24h and 72h after embolization. Pathological examination was performed after chloral hydrate anesthesia, and NF-κB protein expression was analyzed by Western blot. The level of NF-κB positive cells was detected by immunohistochemical staining. RESULTS: Pulmonary histopathology confirmed typical APE thrombosis and alveolar necrosis hemorrhage. CUR treatment can reduce lung tissue lesions. Immunohistochemical staining showed that there were different degrees of NF-κB protein expression around alveolar cells, macrophages, bronchial epithelial cells and bronchial smooth muscle. At 6 h, 24 h, and 72 h after embolization, the number of NF-κB positive cells in the CUR-treated group was significantly lower than that in the model group (P<0.001), and was close to the control and sham-operated groups. At 6 h and 24 h after embolization, Western blot showed that the expression of NF-κB protein was lower in the CUR group than in the model group (P<0.01), and it was close to the control and sham group. Conclusion: CUR can improve lung damage by down-regulating the expression of NF-κB transcription factor in lung tissue of APE rats, which may be one of the mechanisms of its intervention in APE.
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