Effect of Qibai Pingfei capsule medicated serum on protein expressions of KATP channel in pulmonary arterial smooth muscle cells via nitric oxide.
10.19540/j.cnki.cjcmm.2017.0059
- Author:
Jie ZHU
1
;
Ze-Geng LI
2
;
Bao-Qin WANG
3
;
Xiang-Li TONG
3
;
Qing-He PENG
1
Author Information
1. School of Integrated Traditional Chinese & Western Medicine, Anhui University of Chinese Medicine, Hefei 230038, China.
2. Anhui University of Chinese Medicine, Hefei 230038, China.
3. The First Affiliated Hospital, Anhui University of Chinese Medicine, Hefei 230031, China.
- Publication Type:Journal Article
- Keywords:
ATP-sensitive potassium channel;
medicated serum;
nitric oxide;
pulmonary vascular smooth muscle cells
- From:
China Journal of Chinese Materia Medica
2017;42(7):1376-1381
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the ATP-sensitive potassium channel (KATP channel) protein expressions during different periods under hypoxia condition and explore the effect of Qibai Pingfei capsule medicated serum (hereinafter referred to as QBPF) on the correlation between the protein expressions of KATP channel and nitric oxide in rat pulmonary arterial smooth muscle cells(PASMCs). Qibai Pingfei capsules were given to SD rats via continuous gavage for 10 days to obtain QBPF. Primary rats PASMCs were cultured by the direct adherent culture method. Western blot was applied to detect the protein expression levels of KATP channel (Kir6.1 and SUR2B) in PASMCs. Then the noncompetitive inhibitor of NO synthase--Nω-nitro-L-arginine methyl ester(L-NAME) and KATP channel inhibitor--glyburide(GLYB) were applied respectively to evaluate the effect of QBPF on the protein expressions of KATP channel. The protein expressions of Kir6.1 and SUR2B were increased after 6-hour hypoxia treament, peaked at the 24-hour hypoxia treament, and decreased in both 48-hour and 72-hour hypoxia groups. Especially, QBPF could further up-regulate the Kir6.1 and SUR2B protein expressions under 24-hour hypoxia condition; however, such up-regulation effect could be blocked by KATP channel inhibitor GLYB and NO specific inhibitor L-NAME, indicating that QBPF played the role of opening KATP channel. The regulatory mechanism was probably associated with up-regulating KATP channel protein expression via NO relative pathway, involving pulmonary vasodilation, and thus relieving the occurence and development of COPD.
