芪白平肺胶囊对慢性阻塞性肺疾病痰瘀阻肺证大鼠血清CAM-2和VEGF的影响

目的 观察芪白平肺胶囊对慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)痰瘀阻肺证大鼠血清钙调节蛋白-2(calmodulin-2,CAM-2)和血管内皮生长因子(vascular endothelial growth factor,VEGF)的影响,探究其作用机制.方法 将280只SD大鼠随机分为正常组(60只)、模型组(60只)、芪白平肺胶囊预防组(芪预组,40只)、芪白平肺胶囊治疗组(芪治组,40只)、尼可地尔预防组(尼预组,40只)、尼可地尔治疗组(尼治组,40只).采用连续4周的强迫游泳、烟熏和低氧应激的复合方法复制COPD痰瘀阻肺证大鼠模型.正常组和模型组分别在实验第4周、第8周、第12周各处死20只大鼠,检测血清CAM-2和VEGF水平;芪预组和尼预组均在模型复制同时预防性给药4周,分别在实验第4周、第8周各处死20只大鼠,检测血清CAM-2和VEGF水平;芪治组和尼治组均在模型复制结束后连续给药4周,分别在实验第8周、第12周各处死20只大鼠,检测血清CAM-2和VEGF水平.结果 两因素方差分析结果显示,模型因素和时间因素对大鼠血清CAM-2和VEGF水平的主效应及其交互作用均具有统计学意义(P＜0.05).在实验第4周、第8周、第12周,模型组大鼠血清CAM-2水平均显著低于正常组(P＜0.05),血清VEGF水平均显著高于正常组(P＜0.05).与同时间模型组比较,尼预组和芪预组大鼠血清CAM-2水平显著升高(P＜0.05),而血清VEGF水平显著降低(P＜0.05).与同时间尼预组比较,芪预组CAM-2水平显著升高(P＜0.05),VEGF水平显著降低(P＜0.05).与同一时间模型组比较,芪治组和尼治组大鼠血清CAM-2水平显著升高(P＜0.05),VEGF水平显著降低(P＜0.05);在实验第12周,芪治组大鼠血清VEGF水平显著低于尼治组(P＜0.05).结论 芪白平肺胶囊和尼可地尔预防性给药和治疗性给药均可调节COPD痰瘀阻肺证大鼠血清CAM-2和VEGF的异常,芪白平肺胶囊的远期效应优于尼可地尔.

Effects of Qibai Pingfei Capsule on Serum Calmodulin-2 and Vascular Endothelial Growth Factor in Rats with Chronic Obstructive Pulmonary Disease and Syndrome of Stagnated Phlegm Obstructing Lung

Objective To observe the effects of Qibai Pingfei Capsule (QPC) on serum calmodulin-2 (CAM-2) and vascular endothelial growth factor (VEGF) in rats with chronic obstructive pulmonary disease (COPD) and syndrome of stagnated phlegm obstructing lung, and to investigate its action mechanism. Methods Two hundred and eighty Sprague-Dawley rats were randomly divided into normal group (n=60), model group (n=60), QPC prevention group (n=40), QPC treatment group (n=40), nicorandil prevention group (n=40), and nicorandil treatment group (n=40). Rats with COPD and syndrome of stagnated phlegm obstructing lung were reproduced by forced swimming, fumigation, and hypoxia for 4 consecutive weeks. In the normal group and the model group, twenty rats were sacrificed at week 4, 8, or 12 of the experiment, and the serum levels of CAM-2 and VEGF were determined. In the QPC and nicorandil prevention groups, rats received prophylactic administration of drugs for 4 weeks during model establishment, and rats were sacrificed at week 4 or 8 of the experiment; the serum levels of CAM-2 and VEGF were determined. In the QPC and nicorandil treatment groups, rats received continuous administration of drugs for 4 weeks after model establishment, and 20 rats were sacrificed at week 8 or 12 of the experiment; the serum levels of CAM-2 and VEGF were determined. Results According to the results of two-way analysis of variance, two factors, model and time, had significant main effects on serum levels of CAM-2 and VEGF in rats and had significant interaction with each other (P<0.05). At weeks 4, 8, and 12 of the experiment, the serum levels of CAM-2 in the model group were significantly lower than those in the normal group (P<0.05), while the serum levels of VEGF in the model group were significantly higher than those in the normal group (P<0.05). Compared with the model group at the same time points, the QPC and nicorandil prevention groups had significantly higher serum levels of CAM-2 (P<0.05) but significantly lower serum levels of VEGF (P<0.05). Compared with the nicorandil prevention group at the same time points, the QPC prevention group had significantly higher serum levels of CAM-2 (P<0.05) but significantly lower serum levels of VEGF (P<0.05). Compared with the model group at the same time points, the QPC and nicorandil treatment groups had significantly higher serum levels of CAM-2 (P<0.05) but significantly lower serum levels of VEGF (P<0.05). At week 12 of the experiment, the QPC treatment group had significantly lower serum levels of VEGF than the nicorandil treatment group (P<0.05). Conclusion The prophylactic or therapeutic administration of QPC or nicorandil can regulate the abnormality of serum CAM-2 and VEGF in rats with COPD and syndrome of stagnated phlegm obstructing lung. QPC achieves better long-term outcomes than nicorandil.