益气化痰方对慢性阻塞性肺疾病大鼠肺泡灌洗液中AQP5、TNF-α和MUC5AC的影响

【目的】观察益气化痰方对慢性阻塞性肺疾病(COPD)大鼠肺泡灌洗液(BALF)水通道蛋白5(AQP5)及其上游信号通道调节因子肿瘤坏死因子-α(TNF-α)和下游信号通道调节因子黏蛋白5AC(MUC5AC)的调节作用。【方法】选用SD大鼠,随机分为空白组,模型组,益气化痰方低、中、高剂量组(剂量分别为7.398、36.99、73.98 g·kg-1·g-1)。除空白组外,其他组均采用香烟熏结合脂多糖气管滴入法复制COPD大鼠模型。采用益气化痰中药煎剂治疗COPD大鼠30 d后取材,观察肺组织苏木精—伊红(HE)染色,采用免疫组织化学法观察AQP5、TNF-α、MUC5AC的表达,酶联免疫吸附法(ELISA)测定大鼠肺泡灌洗液(BALF)中AQP5、TNF-α和MUC5AC的含量。【结果】益气化痰汤各剂量组均可改善COPD大鼠的肺组织病理损害,减弱肺组织MUC5AC、TNF-α表达,增强AQP5表达。与空白组比较,模型组肺组织BALF中AQP5浓度显著下降(P0.01),TNF-α和MUC5AC浓度显著升高(P0.01)。与模型组比较,益气化痰方低、中、高剂量组肺组织BALF中AQP5浓度显著升高(P0.01),TNF-α和MUC5AC浓度显著下降(P0.01)。与低、中剂量组比较,益气化痰汤高剂量组作用显著(P0.01)。【结论】益气化痰方对COPD的疗效可能与水通道转运密切相关。

Effect of Yiqi Huatan Decoction on Aquaporin 5, Tumor Necrosis Factor-alpha and MUC5AC in Bronchoalveolar Lavage Fluid of Chronic Obstructive Pulmonary Diseases Rats

Objective To investigate Yiqi Huatan Decoction(YHD), a compound recipe with the actions of tonifying Qi and resolving phlegm, on aquaporin 5(AQP5), tumor necrosis factor-alpha(TNF-α)and mucin 5AC(MUC5AC)in bronchoalveolar lavage fluid(BALF)of chronic obstructive pulmonary diseases(COPD)rats. Methods SD rats were randomized into blank control group, model group, and low-, middle- and high-dose YHD groups(in the dosage of 7.398, 36.99, 73.98 g·kg-1·d-1 respectively). The rat model of COPD was induced by cigarette smoking combined with intratracheal dripping of lipopolysaccharide(LPS). After COPD rats were treated with YHD for 30 days, the histological features of lung tissues were observed after hematoxylin-eosin (HE) staining, the expression of AQP5, TNF -α and MUC5AC in the lung tissue was detected by immunohistochemistry, the concentrations of AQP5, TNF-α and MUC5AC in BALF of rats were measured by enzyme-linked immunosorbent assay(ELISA). Results Compared with the blank control group, the concentration of AQP5 in BALF of the model group was decreased significantly(P<0.01), while the concentrations of TNF-αand MUC5AC were significantly increased(P<0.01). Compared with the model group, the pathological features of the lung tissue were relieved, and the concentration of AQP5 was increased significantly in low-, middle-, high-dose YHD groups (P<0.01), but the concentrations of TNF-α and MUC5AC were significantly decreased (P<0.01), and the effect of high-dose group was superior to low-and middle-dose groups(P<0.01). Conclusion The therapeutic mechanism of YHD for COPD is probably related with the regulation of fluid transport in aquaporin water channels of rats.