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目的:探讨山柰酚是否通过下调转录因子NF-κB信号通路的表达而保护感染猪源甲型H9N2流感病毒引起急性肺损伤的小鼠。方法:猪源甲型H9N2流感病毒感染BALB/c小鼠建立急性肺损伤模型,山柰酚干预后检测肺湿重与干重比,观察肺组织的病理学变化,检测支气管肺泡灌洗液内炎性细胞数量以及肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)和白细胞介素1β(IL-1β)含量同时检测肺组织匀浆中超氧化物歧化酶(SOD)和髓过氧化物酶(MPO)活性以及丙二醛(MDA)含量,Western blot检测小鼠肺内NF-κB P65的表达,ELISA检测小鼠肺组织匀浆细胞核提取物中NF-κB P65和NF-κB P50的核转位。结果:山柰酚能降低小鼠死亡率,改善肺组织的病理学变化和肺水肿程度,并能降低肺内巨噬细胞、淋巴细胞和中性粒细胞等炎性细胞的数量同时降低TNF-α、IL-6、IL-1β和MDA的含量,抑制MPO的活性并升高SOD的活性。另外,山柰酚可以下调NF-κB P65的表达增加细胞核提取物中NF-κB P65和NF-κB P50的核转位。结论:山柰酚通过下调NF-κB信号通路的表达从而降低猪源甲型H9N2流感病毒所致急性肺损伤小鼠的炎症程度和氧化应激损伤,最终减轻流感病毒所致的急性肺损伤。
AIM: To investigate whether kaempferol protects mice from acute lung injury induced by swine influenza A (H9N2) virus by down-regulating NF-κB signaling pathway. Methods: Acute lung injury (BALF) was induced in BALB / c mice infected with swine influenza A (H9N2) virus. The ratio of wet weight to dry weight was determined after the intervention of kaempferol. The pathological changes in lung tissue were observed. The intranasal bronchoalveolar lavage fluid Inflammatory cells and levels of tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6) and interleukin 1β (IL-1β) in lung homogenates were measured simultaneously. The levels of superoxide dismutase Myeloperoxidase (MPO) activity and malondialdehyde (MDA) content in the lung were detected by Western blot. The expression of NF-κB P65 and NF-κB in the lung tissue homogenate were detected by ELISA. Nuclear translocation of -κB P50. Results: The kaempferol can reduce the mortality of mice, improve the pathological changes of lung tissue and the degree of pulmonary edema, and can reduce the number of inflammatory cells such as macrophages, lymphocytes and neutrophils in the lungs, α, IL-6, IL-1β and MDA, inhibit the activity of MPO and increase the activity of SOD. In addition, kaempferol down-regulated the expression of NF-κB P65 and increased nuclear translocation of NF-κB P65 and NF-κB P50 in nuclear extracts. CONCLUSION: The kaempferol can reduce the degree of inflammation and oxidative stress in mice with acute lung injury induced by swine influenza A (H9N2) virus by down-regulating the expression of NF-κB signaling pathway and ultimately reduce the acute lung injury induced by influenza virus.