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目的:探讨清肺通络敷胸膏对流感病毒肺炎大鼠肺组织中c-Jun氨基末端激酶(JNK),丝裂原活化蛋白激酶激酶4(MKK4)表达的影响,并探讨其作用机制。方法:幼龄Wistar大鼠随机分为正常组、模型组、敷胸膏高、中、低剂量组(21.0,10.5,5.25 g·kg-1),每组10只。除正常组外,其余各组采用甲型流感病毒鼠肺适应株A/FM/47(H1N1)0.1 m L滴鼻建立流感病毒肺炎模型,造模成功后各治疗组给予不同剂量敷胸膏治疗5 d。苏木素-伊红(HE)染色观察各组大鼠肺组织病理变化,免疫组化检测大鼠肺组织中JNK及MKK4的蛋白表达,实时荧光定量聚合酶链式反应(Real-time PCR)进一步检测肺组织中JNK及MKK4 mRNA表达水平。结果:HE染色结果提示,与模型组比较,敷胸膏高、中、低剂量组能明显改善流感病毒肺炎大鼠肺组织损伤程度,随剂量增大而逐渐增强。免疫组化与Resl-time PCR结果显示,与正常组比较,模型组JNK,MKK4蛋白及mRNA表达显著增强(P<0.05);与模型组比较,敷胸膏高、中、低剂量组JNK,MKK4蛋白及mRNA表达均显著减弱(P<0.05)。结论:敷胸膏对流感病毒肺炎大鼠的保护作用机制可能与下调MAPKs信号通路中JNK,MKK4的表达有关。
Objective: To investigate the effect of Qingfei Tongluo Chest Paste on the expression of c-Jun N-terminal kinase (JNK) and mitogen-activated protein kinase kinase 4 (MKK4) in the lung tissue of influenza virus pneumonia rats and to explore its mechanism. Methods: The young Wistar rats were randomly divided into normal group, model group, high, medium and low dose chest cream group (21.0,10.5,5.25 g · kg-1), 10 in each group. In addition to the normal group, influenza virus pneumonia model was established by intranasal influenza A virus vaccine strain A / FM / 47 (H1N1) 0.1 mL intranasally in all the other groups. After the model was established, the patients in each treatment group were given different doses of chest cream 5 d. The hematoxylin-eosin (HE) staining was used to observe the pathological changes of lung tissue in each group. The protein expressions of JNK and MKK4 were detected by immunohistochemistry and real-time PCR Lung tissue JNK and MKK4 mRNA expression levels. Results: The results of HE staining suggested that compared with the model group, the high, middle and low dose chest cream group could significantly improve the degree of lung injury in influenza virus pneumonia rats, and gradually increased with dose. The results of immunohistochemistry and Resl-time PCR showed that compared with normal group, the expression of JNK and MKK4 protein and mRNA in model group were significantly increased (P <0.05). Compared with model group, JNK, MKK4 protein and mRNA expression were significantly decreased (P <0.05). Conclusion: The protective mechanism of Fuzhibao on influenza virus pneumonia in rats may be related to the downregulation of JNK and MKK4 in MAPKs signaling pathway.