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目的:探究清肺通络膏对流感病毒诱导的肺炎大鼠肺组织中PI3K/AKT/NF-KB信号传导通路的调控机制。方法:将40只Wistar大鼠随机分为正常组,模型组,清肺通络膏高、中、低剂量组,除正常组外,采用鼻腔接种流感病毒FM1株诱导Wistar幼龄大鼠肺炎,在感染后各治疗组采用清肺通络膏贴敷于大鼠背部肺脏投影区治疗。观察各组大鼠的一般状态;肺组织形态学;采用免疫组化染色法检测各组大鼠肺组织PI3K,AKT,核因子NFB p65的表达水平。结果:与正常组相比,模型组大鼠肺组织中PI3K,AKT,NF-k B p65的表达显著增高(P<0.05),清肺通络膏高剂量组PI3K,AKT,NF-k B p65的表达较模型组明显降低(P<0.05)。结论:清肺通络膏通过抑制PI3K/AKT信号通路,使NF-k B p65表达降低,从而减轻了肺组织的病理损伤,达到治疗目的。
Objective: To investigate the regulatory mechanism of Qingfei Tongluo Paste on PI3K / AKT / NF-KB signal transduction pathway in lung tissue of rats with pneumonia induced by influenza virus. Methods: Forty Wistar rats were randomly divided into normal group, model group and Qingfei Tongluo cream high, medium and low dose groups. In addition to the normal group, intranasal influenza virus FM1 strain was used to induce pneumonia in Wistar rats, After infection, each treatment group was treated with Qingfei Tongluo Paste in the back of the lung projection area of rats. The general state of the rats in each group was observed. The lung histomorphology was observed. The expression of PI3K, AKT, nuclear factor NFB p65 in the lung tissue of each group was detected by immunohistochemical staining. Results: Compared with the normal group, the expression of PI3K, AKT and NF-κB p65 in the model group was significantly increased (P <0.05), and the expression of PI3K, AKT, NF-κB The expression of p65 was significantly lower than the model group (P <0.05). Conclusion: Qingfei Tongluo Tong can reduce the expression of NF-κB p65 by inhibiting the PI3K / AKT signaling pathway, thereby reducing the pathological damage of lung tissue and achieving the therapeutic goal.