1. 天津中医药大学第二附属医院
2. 天津中医药大学
纸质出版:2016
移动端阅览
[1]封继宏,祁海燕,李美凤,郑兆晔,刘伟,苏景深,关鹏,杨爽,李云辉,孙增涛.扶正祛邪方对慢性阻塞性肺疾病稳定期模型大鼠肺组织细菌菌落的影响[J].中医杂志,2016,57(04):337-341.
FENG Jihong, QI Haiyan, LI Meifeng, et al. Effect of Fuzheng Quxie Prescription( 扶正祛邪方) on Lung Tissue Bacterial Colony in Model Rats with Chronic Obstructive Pulmonary Disease In Stable Phase[J]. Journal of Traditional Chinese Medicine2016, 57(4): 337-341.
[1]封继宏,祁海燕,李美凤,郑兆晔,刘伟,苏景深,关鹏,杨爽,李云辉,孙增涛.扶正祛邪方对慢性阻塞性肺疾病稳定期模型大鼠肺组织细菌菌落的影响[J].中医杂志,2016,57(04):337-341. DOI: 10.13288/j.11-2166/r.2016.04.017.
FENG Jihong, QI Haiyan, LI Meifeng, et al. Effect of Fuzheng Quxie Prescription( 扶正祛邪方) on Lung Tissue Bacterial Colony in Model Rats with Chronic Obstructive Pulmonary Disease In Stable Phase[J]. Journal of Traditional Chinese Medicine2016, 57(4): 337-341. DOI: 10.13288/j.11-2166/r.2016.04.017.
目的探讨扶正祛邪方治疗慢性阻塞性肺疾病(COPD)稳定期的可能作用机制。方法将56只Wistar大鼠随机分为对照组、模型组、扶正祛邪组和抗生素组
每组14只。除对照组外
其余各组均采用气管内滴注弹性蛋白酶和细菌建立COPD稳定期大鼠模型。造模后对照组、模型组采用灭菌生理盐水2 ml灌胃;扶正祛邪组给予扶正祛邪方0.95 g/(kg·d)灌胃
各组均每日1次
连续1个月;抗生素组给予盐酸莫西沙星片40 mg/(kg·d)灌胃
每天1次
连续3天
每周重复1次
共4次。治疗前后分别观察肺组织病理、肺组织细菌菌落计数
检测大鼠血清Toll样受体4(TLR4)、核因子κB(NF-κB)、β防御素-2(h BD-2)含量。结果病理结果显示
模型组镜下可见支气管上皮细胞部分变形坏死
部分脱落
肺泡腔增大
肺泡壁变薄
周围多处可见大量炎性细胞浸润;各药物干预组镜下均见不同程度肺泡结构紊乱
肺泡腔增大
肺泡壁变薄
肺泡融合
周围可见少量炎性细胞。治疗前后对照组大鼠肺组织匀浆未分离出细菌
模型组及各治疗组均不同程度分离出细菌
且各治疗组细菌菌落计数较本组治疗前有下降趋势。与对照组比较
模型组大鼠给药前后血清中TLR4、NF-κB、h BD-2均明显升高(P<0.05);扶正祛邪组、抗生素组给药前血清中TLR4、NF-κB、h BD-2亦明显高于对照组
而给药后血清中TLR4、NF-κB、h BD-2含量较模型组给药后及本组给药前明显降低(P<0.05)。结论扶正祛邪方治疗COPD稳定期可能是通过调节TLR4/NF-κB/h BD-2信号转导通路
调节免疫炎症反应
相对提高下呼吸道细菌负荷阈值
进而减轻病原体的损害。
Objective To explore the possible mechanism of Fuzheng Quxie Prescription in the treatment of chronic obstructive pulmonary disease in stable phase. Methods Fifty sixty Wistar rats were randomly divided into control group
model group
Fuzheng Quxie group and the antibiotic group
with 14 rats in each group. Except the control group
in the other groups
intratracheal instillation of elastase and bacteria were given to establish rat model with chronic obstructive pulmonary disease in stable phase. After model establishment
the control group and the modelgroup were gavaged with 2 ml of sterile saline; Fuzheng Quxie group was gavaged with 0. 95 g /( kg · d) of Fuzheng Quxie Prescription
and all the groups were treated one time a day for one month. Antibiotic group was gavaged with 40 mg /( kg·d) of moxifloxacin hydrochloride tablet
one time a day for 3 days
with one week as a circle
altogether for 4 circles. The pathology and the bacterial colony count of the lung tissue were examined before and after treatment
and the content of rat serum Toll like receptor 4( TLR4)
nuclear factor κ B( NF-κB)
β-defensins-2( h BD-2) were detected. Results The pathological results showed that
in the model group
there were partial deformation
necrosis
and loss in bronchial epithelial cells
alveolar cavity enlargement
and the thinner alveolar
and a large number of inflammatory cell infiltration could be seen around; In each drug intervention group
there were different degree of alveolar structure disorder
alveolar cavity enlargement
the thinner alveolar wall
and alveolar fusion
and a small amount of inflammatory cells could be seen around. There were no isolated bacteria from the lung tissue homogenate of rats in control group before and after treatment. In the model group and the treatment groups
more or less bacteria were isolated
and the bacterial colony counts in each drug intervention group had a downward trend compared with those of before treatment. Compared with the control group
the serum levels of TLR4
NF-κB and h BD-2 were significantly increased in the model group before and after treatment( P < 0. 05); Before administration
the serum levels of TLR4
NF-κ B
h BD-2 in Fuzheng Quxie group and antibiotic group were also significantly higher than those in the control group; After administration
the serum levels of TLR4
NF-κB
h BD-2 in these two groups were significantly lower than those before treatment
and also significantly lower than those of the model group after administration( P < 0. 05). Conclusion Fuzheng Quxie Prescription could treat rats with chronic obstructive pulmonary disease in stable phase possibly through adjusting TLR4 / NF-κB / h BD-2 signal transduction pathway
regulating the immune inflammatory response
relatively increasing the lower airway tract bacterial load threshold
thus to reduce the damage of pathogens.
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