Zhang Wei, Liu Hai-yu
Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan.
Zhongguo Zhong Xi Yi Jie He Za Zhi. 2009 Jan;29(1):51-4.
To research the influence of pathogenic dampness on changes of cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), interluekin-4 (IL-4), interferon-gamma (IFN-gamma), etc. in the lung of rats with different gradients of evil-cold invading Fei. Methods One hundred and four Wistar rats of SPF grade were randomized depending on the digital table into 13 groups, 8 in each group: the normal temperature group, the 6 evil-cold invasive groups (ECG1-6) and the 6 cold-dampness invasive groups (CDG1-6). Rats in the ECG and CDG groups were exposed to cold or cold-dampness to different gradients, for subgroups 1 to 6, -10 degrees C, 0 degrees C, 10 degrees C, 20-10 degrees C, 20-0 degrees C and 20 - -10 degrees C was applied respectively for 2 h, then fed at room temperature to observe their general condition. Rats were sacrificed 4 days later and their lung tissue was taken out for determination of the contents of TNF-alpha, IL-6, IFN-gamma and IL-4 in lung tissue homogenate. Results Compared with the corresponding ECG groups, the contents of TNF-alpha, IL-6 and IL-4 were higher (P < 0.05 or P < 0.01), content of IFN-gamma and IFN-gamma/IL-4 ratio were significantly lower in the CDG groups (P < 0.01).
Pathogenic dampness could aggravate the injury of Fei caused by the pathogenic cold to induce the change of inflammation related cytokines to a certain extent, and the unbalance of Th1/Th2 immune response in organism could be worsened as well.
研究寒湿对不同程度寒邪犯肺大鼠肺组织中肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、白细胞介素-4(IL-4)、干扰素-γ(IFN-γ)等细胞因子变化的影响。方法将104只SPF级Wistar大鼠按随机数字表法分为13组,每组8只:常温组、6个寒邪侵袭组(ECG1 - 6)和6个寒湿侵袭组(CDG1 - 6)。ECG组和CDG组大鼠分别接受不同程度的寒邪或寒湿刺激,1至6亚组分别给予-10℃、0℃、10℃、20 - 10℃、20 - 0℃和20 - -10℃刺激2小时,然后在室温下饲养并观察其一般情况。4天后处死大鼠,取出肺组织,测定肺组织匀浆中TNF-α、IL-6、IFN-γ和IL-4的含量。结果与相应的ECG组相比,CDG组TNF-α、IL-6和IL-4的含量较高(P < 0.05或P < 0.01),IFN-γ含量及IFN-γ/IL-4比值显著降低(P < 0.01)。
寒湿可加重寒邪所致的肺损伤,在一定程度上诱导炎症相关细胞因子的变化,同时也可加剧机体Th1/Th2免疫反应失衡。