黄芩苷对流感病毒PR8感染小鼠内质网应激反应的干预作用  

Effects of a baicalin intervention on endoplasmic reticulum stress in response to infection with the PR8 strain of influenza virus

作　　者：吴彤[1] 牛姝力[1] 白梅[1] WU Tong NIU Shu-li BAI Mei(J inzhou Center For Disease Control and Prevention, J inzhou 121001, Liaoning, China)

机构地区：[1]锦州市疾病预防控制中心,辽宁锦州121000

出　　处：《中国病原生物学杂志》2017年第6期553-556,559,共5页Journal of Pathogen Biology

基　　金：国家重大传染病防治科技重大专项项目(No.2012ZX10004209-001)

摘　　要：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。Objectives To create a mouse model of lung injury induced by the PR8 strain of influenza virus and to de- tect expression of PERK, CHOP, p-JNK, and Caspase-12 in relation to endoplasmic reticulum stress in order to investi- gate the effects of baicalin treatment and to examine its protective effect and mechanism of action. Methods Mice were divided into a control group, a baicalin treatment group, a prophylactic baicalin treatment group, and a ribavirin control group. A model of acute lung injury was created by infection with the A/PR/8/34（H1N1） strain of influenza virus, and treated groups received the corresponding treatment. After treatment with baicalin, pathological changes in lung tissue were observed. The expression of PERK, CHOP, p-JNK, and Caspase-12 in lung tissue was detected using Western blotting. The expression of Caspase-12 was located immunohistochemically. Results The lung index was markedly lower in the baicalin treatment group and prophylactic baicalin treatment group （0.98±0.13 and 1.25±0.14） than that in the PR8 group （1.42±0.11） （F=43. 850, P〈0.01; F=5. 750, P〈0.05）, and pulmonary lesions decreased in those 2 groups. The relative levels of PERK, CHOP, pJNK, and Caspase-12 expression in lung tissue （2.86±0.23, 4.75±0.38, 5.02±0.49, and 3.64±0.36） were significantly higher in the PR8 group than those in the control group （F 156. 650,P〈0.01）. The relative level of PERK expression in the baicalin treatment group was 1.53±0.09, the relative level of CHOP expression was 2.10±0.26, the relative level of p-JNK expression was 2.57±0.33, and the relative level of Caspase 12 expression was 1.75±0.21. The relative level of PERK expression in the prophylactic baicalin treatment group was 1.96±.21, the relative level of CHOP expression was 2.75±0.12, the relative level of p-JNK expression was 3.42±0.34, and the relative level of Caspase-12 expression was 2.44±0.38. Expression of PERK, CHOP, p-JNK, and Caspase-12 was inhibited in the baicalin treatment group and

关 键 词：黄芩苷 流感病毒 PERK CHOP pJNK CASPASE-12 

分 类 号：R373.13[医药卫生—病原生物学]