“痰性粘滞”理论的实验研究  

Investigation of "Phlegm Being Adhesive in Nature"

作　　者：吴建奇[1] 李小兵[2] 

机构地区：[1]广东省第二中医院,广东广州510405 [2]广州中医药大学第一附属医院,广东广州510405

出　　处：《中医学报》2013年第5期688-689,I0001,共3页Acta Chinese Medicine

摘　　要：目的:观察补肺化痰方对肺虚痰阻证模型大鼠肺组织单核细胞趋附因子-1(MCP-1)、血管细胞黏附分子-1(VCAM-1)及黏附分子-1(ICAM-1)的影响,从而探讨痰性粘滞的机理。方法:将40只SD大鼠按随机数字表单盲法分为模型组19只和治疗组21只,采用冷风刺激加烟熏法建立大鼠肺虚痰阻证模型,治疗组给予补肺化痰方灌胃,模型组给予等体积生理盐水,共14 d。观察各组大鼠一般活动情况、浓氨水刺激后3 min内咳嗽只数、大鼠肺组织病理改变及MCP-1、VCAM-1及ICAM-1的变化。结果:3 min内模型组咳嗽大鼠例数与治疗组比较,差异有统计学意义(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;治疗组细胞间ICAM-1及VCAM-1、MCP-1都明显高于模型组(P<0.05)。结论:补肺化痰方可减少肺虚痰阻证模型大鼠肺组织中MCP-1、ICAM-1和VCAM-1的含量,黏附分子、趋化因子介导细胞与细胞间、细胞与基质间或细胞-基质-细胞间的黏附,及其引起的气道黏液高分泌可能是痰邪致病特点。Objective ：To observe the effects of reinforcing lung prescription on MCP-1, VCAM-1 and ICAM-1 of lung asthenia model rats to explore the mechanism of viscous phlegm. Methods ：40 SD rats were randomly divided into model group（ n = 19 ） and treatment group （n = 21 ）. Establish the rats model of lung asthenia and phlegm stagnation using cold stimulation and smudging. The treatment group was given intragastric administration of reinforcing lung prescription and the model group was given equal volume of normal saline, 14D. Ob- serve the general activities,cough numbers after 3 min with ammonia stimulation, pathological changes of rat lung tissue and MCP-1, VCAM-1 and ICAM-1 changes. Resuhs：Compared the cough numbers in 3 rain,the difference was statistically significant （P 〈 0.05 ）. The pathological sections showed the trachea, bronchial goblet cell proliferation, adenoid hypertrophy and hyperplasia in treatment group were better than those of model group. The intercellular adhesion molecule-1 （ ICAM-1 ）, vascular cell adhesion molecule -1 （ VCAM-1 ） and monocyte ingratiate oneself factor -1 （ MCP-1 ） were significantly higher than those in model group （ P 〈 0.05 ）. Conclusion ： Rein- forcing lung prescription can reduce the content of MCP-1 ,ICAM-1 and VCAM-1 in lung tissue.

关 键 词：肺虚痰阻证 痰性粘滞 黏附分子 趋化因子 大鼠 

分 类 号：R285.5[医药卫生—中药学]