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目的:研究槐定碱对内毒素(LPS)致小鼠肺损伤(ALI)的抗氧化作用及对核因子kappa B(NF-κB)表达的影响。方法:将清洁级昆明小鼠60只分为6组:正常组、LPS模型组、ip槐定碱5 mg.kg-1预防给药组、槐定碱高、中、低剂量治疗组(9,5,2.5 mg.kg-1),每组10只。预防给药组造模前连续3 d ip给予小鼠槐定碱;槐定碱治疗组均在造模后连续3 d ip给予小鼠槐定碱;观察小鼠用药前后的一般状况、肺组织匀浆超氧化物歧化酶(SOD)和丙二醛(MDA)含量变化、肺组织病理形态学改变及免疫组化检测肺组织中NF-κB p65的表达。结果:槐定碱中、低剂量组和预防给药组,均不同程度改善了模型鼠的一般状况,并可不同程度地升高肺匀浆SOD活力(P<0.05),降低肺匀浆MDA含量(P<0.05),减轻肺组织的氧化病理损伤;槐定碱高、中、低剂量组和预防给药组明显降低了小鼠肺组织细胞中NF-κB p65的表达,且槐定碱中剂量组作用效果最显著。结论:槐定碱可不同程度地减轻内毒素致肺损伤模型鼠的病理损害,对氧自由基引起的损伤具有一定的保护和治疗作用;通过下调模型小鼠肺组织中NF-κB的表达,而阻断LPS信号转导途径中Toll样受体4*(TLR-4)介导的NF-κB通路。
OBJECTIVE: To study the anti-oxidative effect of sophoridine on lung injury (ALI) induced by endotoxin (LPS) and its effect on the expression of nuclear factor kappa B (NF-κB) in mice. Methods: Sixty clean Kunming mice were divided into 6 groups: normal group, LPS model group, ip sophoridine 5 mg.kg-1 prophylaxis group, sophoridine high, medium and low dose treatment group (9 , 5, 2.5 mg.kg-1), 10 in each group. The mice in the preventive group were given sophoridine for 3 consecutive days before modeling. The rats in the sophoridine group were given sophoridine for 3 consecutive days after modeling. The general condition of the mice before and after the treatment was observed. The lung tissues The contents of superoxide dismutase (SOD) and malondialdehyde (MDA) in the homogenate were determined. The pathological changes of lung tissue and the expression of NF-κB p65 in lung tissue were detected by immunohistochemistry. Results: Sophoridine low dose group and prophylaxis group all improved the general status of model rats to varying degrees, and increased SOD activity (P <0.05) and decreased MDA content (P <0.05), and alleviated the oxidative pathological damage of lung tissue. The sophoridine high, medium and low dose groups and prophylaxis administration group significantly reduced the expression of NF-κB p65 in mouse lung tissue, and sophoridine The effect of the middle dose group is the most significant. CONCLUSIONS: Sophoridine can alleviate the pathological damage induced by endotoxin-induced lung injury to some degree and protect and treat the injury induced by oxygen free radicals. By down-regulating the expression of NF-κB in the lung tissue of model mice, While blocking the TLR-4-mediated NF-κB pathway in the LPS signaling pathway.