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目的探讨肺虚痰阻证模型大鼠Na+-K+-ATP酶活性变化及补肺化痰方的干预效果。方法 30只SD大鼠随机分为正常组、模型组和治疗组各10只,采用冷风刺激加烟熏法致大鼠肺虚痰阻证模型,治疗组给予补肺化痰方,正常组和模型组给予等体积生理盐水,共14天。观察各组大鼠一般活动情况、浓氨水刺激后3min内咳嗽次数、大鼠肺组织病理改变及Na+-K+-ATP酶活性变化。结果用浓氨水刺激诱发咳嗽后,3min内模型组及治疗组咳嗽次数较正常组增加(P<0.05);治疗组大鼠病理切片示气管、支气管杯状细胞增生,腺体肥大、增生均较模型组减轻;模型组和治疗组的Na+-K+-ATP酶活性均低于正常组(P<0.05),但治疗组明显高于模型组(P<0.05)。结论补肺化痰方可上调肺虚痰阻证模型大鼠Na+-K+-ATP酶活性,肺泡膜上Na+-K+-ATP酶的活性降低可能是产生肺虚痰阻证的机制之一。
Objective To investigate the change of Na+-K+-ATPase activity in the model rats with deficiency of lung and the effect of Bufei Huayu Decoction. Methods Thirty male Sprague-Dawley rats were randomly divided into normal group, model group, and treatment group. Ten rats were treated with cold wind stimulation plus smoking method. The rats in the treatment group were given Bufei Huayu Decoction. The model group was given an equal volume of saline for a total of 14 days. Observe the general activity of rats in each group, the number of coughs within 3 minutes after concentrated ammonia stimulation, the pathological changes of lung tissue and Na+-K+-ATPase activity changes. Results After cough induced by concentrated ammonia stimulation, the number of cough in the model group and the treatment group was increased in 3 min compared with the normal group (P<0.05). The pathological section of the treated group showed trachea, bronchial goblet cell hyperplasia, glandular hypertrophy, and hyperplasia. The model group was relieved; the Na+-K+-ATPase activity in the model group and the treatment group was lower than the normal group (P<0.05), but the treatment group was significantly higher than the model group (P<0.05). Conclusion Bufei Huatan Decoction can upregulate Na+-K+-ATPase activity in model rats with deficiency of lung and sputum, and the decrease of Na+-K+-ATPase activity in the alveolar membrane may be one of the mechanisms of lung deficiency syndrome.