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目的观察黄芩苷(Baicalin)对流感病毒PR8感染小鼠急性肺损伤内质网应激相关蛋白PERK、CHOP、pJNK及Caspase-12表达的影响,探讨其对PR8小鼠感染急性肺损伤的保护作用及机制。方法实验分为健康对照组,PR8组,黄芩苷治疗组,黄芩苷预防给药组,利巴韦林治疗对照组。用流感病毒鼠肺适应株A/PR/8/4(H1N1)建立小鼠流感病毒性肺炎模型后按相应治疗方案进行给药治疗,观察小鼠肺组织病理变化,应用Western blot法检测PERK、CHOP、p-JNK及Caspase-12蛋白水平。结果黄芩苷治疗和预防给药肺指数(0.98±0.13、1.25±0.14)较比PR8组(1.42±0.11)明显降低(F=43.850,P<0.01;F=5.750,P<0.05),肺组织病变减轻;黄芩苷治疗和预防给药组各指标相对表达量分别为PERK(1.53±0.09、1.96±0.21)、CHOP(2.10±0.26、2.75±0.12)、pJNK(2.57±0.33、3.42±0.34)及Caspase-12(1.75±0.21、2.44±0.38),与PR8组(2.86±0.23、4.75±0.38、5.02±0.49、3.64±0.36)相比,表达量显著下降(F=135.340,P<0.01;F=74.100,P<0.01)。结论黄芩苷治疗和预防给药均能缓解甲型流感病毒PR8诱导的小鼠肺炎性病理损伤,通过下调内质网应激反应和抑制组织细胞的凋亡,发挥抗流感病毒感染的作用。
Objective To investigate the effect of Baicalin on the expressions of PERK, CHOP, pJNK and Caspase-12 in acute lung injury induced by influenza virus PR8 in mice and the protective effect of Baicalin against PR8-infected acute lung injury And mechanism. Methods The experiment was divided into healthy control group, PR8 group, baicalin treatment group, baicalin preventive treatment group and ribavirin treatment control group. The mouse model of influenza virus pneumonia was established with influenza virus murine lung-adapted strain A / PR / 8/4 (H1N1), then the mice were treated with the corresponding treatment regimen. The pathological changes in the lung tissue were observed and the expression of PERK, CHOP, p-JNK and Caspase-12 protein levels. Results Compared with PR8 group (1.42 ± 0.11), the lung index (0.98 ± 0.13,1.25 ± 0.14) of baicalin treatment and prophylaxis was significantly lower (F = 43.850, P <0.01; F = 5.750, P < The relative expression of each index in the baicalin treatment and prophylaxis groups were respectively PERK (1.53 ± 0.09,1.96 ± 0.21), CHOP (2.10 ± 0.26, 2.75 ± 0.12), pJNK (2.57 ± 0.33, 3.42 ± 0.34) (1.75 ± 0.21, 2.44 ± 0.38), respectively. Compared with PR8 group (2.86 ± 0.23,4.75 ± 0.38,5.02 ± 0.49,3.64 ± 0.36), the expression of Caspase-12 decreased significantly (F = 135.340, F = 74.100, P <0.01). Conclusion Both baicalin and prophylaxis can alleviate pneumonia pathological damage induced by influenza A virus PR8 in mice and exert anti-influenza virus infection by down-regulating ER stress and inhibiting apoptosis of tissue cells.