温燥致病机制的实验研究

目的研究温燥对小鼠的主要致病机制。方法273只昆明种小鼠随机分为常温常湿组、常温燥组、温燥组,每组91只,在模拟温燥条件下造模,第7天与第14天分别进行气道与皮肤组织病理、气道液IgG抗体(IgG-R)、血液流变学、细菌攻击试验、气管细胞bcl-2、bax基因表达的检测。结果与常温常湿组相比,温燥组气管、肺与皮肤病变明显,肺细菌数增高,IgG-R持续降低与血浆黏度增高(P<0.01),气管细胞bcl-2表达下降。结论温燥灼肺伤津,致气道IgG抗体持续降低与"纤毛-黏液毯"局部御邪屏障受损;津伤则生血不足,继之血液黏度增高;肺津宣输失司则皮肤"枯、涸、皴、揭",为温燥致病提供组织学基础。

Experimental Study on the Mechanism of Warm-dryness in Causing Diseases

Objective To study the main mechanism of pathogenic warm-dryness in causing diseases to mice.Methods The 216 Kunming species mice were randomized into normal temperature and humidity group, normal temperature and dryness group, and warm dryness group with 72 in each. The models were made under the simulated condition of warm-dryness. On the 7th day and 14th day, the observation on pathological changes of air passage and skin tissues, IgG-R of fluid of air passage, hemorrheology, bacteria attack experiment, and expression of bcl-2 and bax was carried out.Results Compared with the normal temperature and humidity group, in the warm dryness group the pathological changes of trachea, lung and skin tissues were obvious, the lung bacterial content increased, IgG-R decreased continuously, and plasma viscosity increased (P<0.01), and expression of bcl-2 decreased.Conclusion The pathogenic warm-dryness damages the lung and consumes its body fluid, causing the IgG of fluid of air passage decreased and the resistance of "ciliary-mucus blanket" injured; the damaged body fluid gives rise to insufficient blood production, leading to the increased plasma viscosity; the failure of lung to disperse the body fluid induces the skin dried up, prepared the histological basis for the invasion of warm-dryness.