Zhu Jie, Wang Baoqin, Lu Mei, Tong Jiabing, Yang Cheng, Li Zegeng
Hubei University of Chinese Medicine, Wuhan, China / Anhui University of Chinese Medicine, Hefei, China.
Anhui University of Chinese Medicine, Hefei, China.
Pak J Pharm Sci. 2018 Mar;31(2):545-552.
This research explores the effects of Qibaipingfei (QBPF) capsules on pulmonary vascular relaxation in vitro and the relationship of the ATP-sensitive K (KATP) channel and nitric oxide (NO) pathway. Vasodilator effects of QBPF (0.125-2 g/kg) on rat pulmonary artery rings were observed using a multi-wire myograph system. The maximum relaxation (E) of QBPF was detected following treatment involving endothelial denudation, Nω-nitro-L-arginine methyl ester (L-NAME), 1H-[1,2,4] oxadiazolo[4,3-α]quinoxalin-1-one (ODQ), or glyburide (GLYB). Furthermore, rat models of phlegm and blood stasis syndrome combined with chronic obstructive pulmonary disease (COPD) were established using compound factors. KIR6.1 and SUR2B protein expression was analyzed by western blotting. After 9,11-dideoxy-11-α],9-α]-epoxy-methanoprostaglandinF (U46619) was used to pre-constrict endothelium-intact pulmonary artery rings, QBPF induced the effects of concentration-dependent relaxation at a concentration for 50% of maximal effect (EC) of 0.56 g/L and E of 84.30% ± 6.27%. After the endothelium was denuded, the vasodilator effects reduced significantly (P<0.01). QBPF-induced relaxation was inhibited by L-NAME, ODQ, and GLYB (P<0.01). The vasodilator effect was also attenuated in the model group (E=62.63%±10.02, EC = 0.72 g/L, P<0.01). In comparison with expression in the control group, SUR2B protein expression was down-regulated in the model group (P<0.01) but no significant difference was detected in KIR6.1 protein expression between the groups (P>0.05). QBPF and nicorandil (Nic) treatment up-regulated SUR2B K channel expression (P<0.05). QBPF induces endothelial-dependent relaxation in pulmonary artery rings in vitro, through a mechanism that potentially activates the K channel in pulmonary vascular smooth muscles via the NO-cyclic GMP (cGMP)-dependent pathway.
本研究探讨七白平肺（QBPF）胶囊对体外肺血管舒张的影响以及三磷酸腺苷敏感性钾（KATP）通道与一氧化氮（NO）途径之间的关系。使用多线肌张力测定系统观察QBPF（0.125 - 2 g/kg）对大鼠肺动脉环的血管舒张作用。在进行内皮剥脱、Nω-硝基-L-精氨酸甲酯（L-NAME）、1H-[1,2,4]恶二唑并[4,3-α]喹喔啉-1-酮（ODQ）或格列本脲（GLYB）处理后，检测QBPF的最大舒张率（E）。此外，采用复合因素建立痰瘀证合并慢性阻塞性肺疾病（COPD）大鼠模型。通过蛋白质印迹法分析KIR6.1和SUR2B蛋白表达。在用9,11-二脱氧-11-α],9-α]-环氧甲撑前列腺素F（U46619）预收缩内皮完整的肺动脉环后，QBPF在浓度为最大效应的50%（EC）为0.56 g/L时诱导浓度依赖性舒张效应，E为84.30%±6.27%。内皮剥脱后，血管舒张作用显著降低（P<0.01）。L-NAME、ODQ和GLYB抑制QBPF诱导的舒张（P<0.01）。模型组的血管舒张作用也减弱（E = 62.63%±10.02，EC = 0.72 g/L，P<0.01）。与对照组相比，模型组SUR2B蛋白表达下调（P<0.01），但各组间KIR6.1蛋白表达无显著差异（P>0.05）。QBPF和尼可地尔（Nic）处理上调SUR2B钾通道表达（P<0.05）。QBPF在体外诱导肺动脉环的内皮依赖性舒张，其机制可能是通过NO-环磷酸鸟苷（cGMP）依赖性途径激活肺血管平滑肌中的钾通道。
