Abstract
Background/Aims: Recently, effective and purified ingredients of traditional Chinese medicine (TCM) were extracted to play crucial roles in the treatment of pulmonary diseases. Our previous research focused on TCM drug screening aimed at abnormal airway muscle contraction during respiratory diseases. Coptisine, an effective ingredient extracted from bitter herbs has shown a series of antioxidant, antibacterial, cardioprotective and neuroprotective pharmacological properties. In the current study, we questioned whether coptisine could also participate in asthma treatment through relaxing abnormal contracted mouse airway smooth muscle (ASM). The present study aimed to characterize the relaxant effects of coptisine on mouse ASM and uncover the underlying molecular mechanisms. Methods: To investigate the role of coptisine on pre-contracted mouse ASM, a series of biological techniques, including force measurement and patch-clamp experiments were employed. Results: Coptisine was found to inhibit high K+ or acetylcholine chloride (ACh)-induced pre-contracted mouse tracheal rings in a dose-dependent manner. Further research demonstrated that the coptisine-induced mouse ASM relaxation was mediated by alteration of calcium mobilization via voltage-dependent L-type Ca2+ channels (VDLCCs) and non-selective cation channels (NSCCs). Conclusion: Our data showed that mouse ASM could be relaxed by coptisine via altering the intracellular Ca2+ concentration through blocking VDLCCs and NSCCs, which suggested that this pharmacological active constituent might be classified as a potential new drug for the treatment of abnormal airway muscle contraction.
Highlights
Pulmonary diseases are a series of debilitating, life-threatening respiratory illnesses that have become severe worldwide public health problems and financial burdens [1]
The results showed that acetylcholine chloride (ACh) or high K+ precontracted mouse airway smooth muscle (ASM) could be relaxed by coptisine in a concentration-dependent manner
10 μM nifedipine, a selective blocker of voltage-dependent L-type Ca2+ channel (VDLCC) [22], has a similar inhibitory on high K+-induced steady state contraction in mouse tracheal rings (n=6/6 mice), which confirmed that the contraction was induced via the opening of VDLCCs. These results indicated that coptisine inhibited high K+-induced pre-contraction in a dose-dependent manner
Summary
Pulmonary diseases are a series of debilitating, life-threatening respiratory illnesses that have become severe worldwide public health problems and financial burdens [1]. Excessive cell matrix proliferation, especially the abnormal contraction of airway smooth muscle (ASM) are the main symptoms of pulmonary diseases [3,4,5]. Traditional Chinese medicine (TCM) especially a large number of herbal formulations play important roles in pulmonary diseases treatment [6]. Our previous studies have revealed that quite a few effective ingredients or extracts of TCM could relax abnormal smooth muscle contraction in pulmonary diseases [7,8]. Research about coptisine aimed at ameliorating excessive abnormal contraction in ASM, which is a key symptom of pulmonary disease, has been limited. The purpose of present study was to investigate the roles of coptisine in pulmonary disease treatments with a focus on mouse ASM relaxation. Further research indicated that coptisine exerted its relaxant effects by decreasing intracellular calcium via voltage-dependent L-type Ca2+ channels (VDLCCs) and non-selective cation channels (NSCCs)
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