scholarly journals Pharmacological effects of Pugionium cornutum (L.) Gaertn. extracts on gastrointestinal motility are partially mediated by quercetin

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Chencan Su ◽  
Haoyu Li ◽  
Bang Chen ◽  
Cong Li ◽  
Chunxiao Zhang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Gastrointestinal Motility ◽  
Calcium Influx ◽  
Cell Model ◽  
Petroleum Ether Extract ◽  
Functional Gastrointestinal Disorders ◽  
Water Extract ◽  
Relaxation Effect

Abstract Background The majority of global population suffer from various functional gastrointestinal disorders. Pugionium cornutum (L.) Gaertn. (PCG) is used to relieve indigestive symptoms in traditional Chinese medicine. However, little is known about the effects of bioactive components from PCG extracts on gastrointestinal motility. Methods Crude ethanol extract of PCG (EEP) was prepared from Pugionium cornutum (L.) Gaertn. Different solvents were used to prepare fine extracts from EEP, including water extract of PCG (WEP), petroleum ether extract of PCG (PEEP), dichloromethane extract of PCG (DEP) and ethyl acetate extract of PCG (EAEP). Smooth muscle cell model and colonic smooth muscle stripe model were used to test the bioactive effects and mechanisms of different PCG extracts on contraction and relaxation. Diverse chromatographic methods were used to identify bioactive substances from PCG extracts. Results EEP was found to promote the relaxation of gastric smooth muscle cell and inhibit the contraction of colonic smooth muscle strip. Among the fractions of EEP, EAEP mainly mediated the relaxation effect by stimulating intracellular calcium influx. Further evidences revealed that EAEP was antagonistic to acetylcholine. In addition, COX and NO-GC-PKC pathways may be also involved in EAEP-mediated relaxation effect. Quercetin was identified as a bioactive compound from PCG extract for the relaxation effect. Conclusion Our research supports the notion that PCG extracts promote relaxation and inhibits contraction of gastrointestinal smooth muscle at least partially through the effect from quercetin.

scholarly journals The myogenic response in isolated rat cerebrovascular arteries: smooth muscle cell model

2003 ◽  
Vol 25 (8) ◽  
pp. 691-709 ◽  
Author(s):  
Jin Yang ◽  
John W. Clark ◽  
Robert M. Bryan ◽  
Claudia Robertson
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Cell Model ◽  
Myogenic Response ◽  
Isolated Rat

scholarly journals Nicotine-Induced Airway Smooth Muscle Cell Proliferation Involves TRPC6-Dependent Calcium Influx Via α7 nAChR

2017 ◽  
Vol 43 (3) ◽  
pp. 986-1002 ◽  
Author(s):  
Wei Hong ◽  
Gongyong Peng ◽  
Binwei Hao ◽  
Baoling Liao ◽  
Zhuxiang Zhao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Signaling Pathway ◽  
Muscle Cell ◽  
Calcium Influx ◽  
Airway Remodeling ◽  
Airway Smooth Muscle Cell ◽  
Calcium Entry ◽  
Α7 Nachr

Background/Aims: The proliferation of human bronchial smooth muscle cells (HBSMCs) is a key pathophysiological component of airway remodeling in chronic obstructive pulmonary disease (COPD) for which pharmacotherapy is limited, and only slight improvements in survival have been achieved in recent decades. Cigarette smoke is a well-recognized risk factor for COPD; however, the pathogenesis of cigarette smoke-induced COPD remains incompletely understood. This study aimed to investigate the mechanisms by which nicotine affects HBSMC proliferation. Methods: Cell viability was assessed with a CCK-8 assay. Proliferation was measured by cell counting and EdU immunostaining. Fluorescence calcium imaging was performed to measure intracellular Ca2+ concentration ([Ca2+]i). Results: The results showed that nicotine promotes HBSMC proliferation, which is accompanied by elevated store-operated calcium entry (SOCE), receptor-operated calcium entry (ROCE) and basal [Ca2+]i in HBSMCs. Moreover, we also confirmed that canonical transient receptor potential protein 6 (TRPC6) and α7 nicotinic acetylcholine receptor (α7 nAChR) are involved in nicotine-induced upregulation of cell proliferation. Furthermore, we verified that activation of the PI3K/Akt signaling pathway plays a pivotal role in nicotine-enhanced proliferation and calcium influx in HBSMCs. Inhibition of α7 nAChR significantly decreased Akt phosphorylation levels, and LY294002 inhibited the protein expression levels of TRPC6. Conclusion: Herein, these data provide compelling evidence that calcium entry via the α7 nAChR-PI3K/Akt-TRPC6 signaling pathway plays an important role in the physiological regulation of airway smooth muscle cell proliferation, representing an important target for augmenting airway remodeling.

scholarly journals Histamine H1-receptor-mediated calcium influx in DDT1MF-2 cells

1992 ◽  
Vol 284 (2) ◽  
pp. 425-431 ◽  
Author(s):  
J M Dickenson ◽  
S J Hill
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Cell Line ◽  
Muscle Cell ◽  
Calcium Influx ◽  
Receptor Activation ◽  
Plateau Phase ◽  
H1 Receptor ◽  
Histamine H1 Receptor ◽  
Muscle Cell Line

Undifferentiated monolayers of the hamster vas deferens smooth-muscle cell line, DDT1MF-2, were grown on glass coverslips and loaded with the Ca(2+)-sensitive fluorescent dye fura-2. Stimulation with histamine produced a rapid and maintained increase in intracellular free Ca2+ ([Ca2+]i), with an EC50 of 7.0 +/- 0.7 microM. The initial rise in [Ca2+]i can be attributed to Ca2+ release from intracellular stores, whereas the maintained or plateau phase is due to influx of extracellular Ca2+. The Ca2+ influx associated with the plateau phase required the continued presence of histamine on the receptor, since the H1-antagonist mepyramine (10 microM) attenuated the rise in [Ca2+]i observed when extracellular Ca2+ was re-applied after the cells had been stimulated with histamine, in experiments performed in nominally Ca(2+)-free buffer. Pretreatment with the inorganic Ca(2+)-channel blockers Ni2+ (1 mM) and Co2+ (1 mM) inhibited the influx component, whereas the organic voltage-operated Ca(2+)-channel antagonists nifedipine (10 microM) and PN-200-110 (10 microM) had no effect. These data suggest that histamine stimulates Ca2+ influx through an H1-receptor-activated Ca2+ channel. Experiments with Mn2+ indicated that the receptor-mediated Ca(2+)-influx pathway(s) is impermeable to Mn2+. Furthermore, the refilling of Ca2+ stores can occur independently of H1-receptor-mediated influx, since store refilling can be demonstrated even when the receptor-mediated Ca2+ entry is blocked by mepyramine. In conclusion, H1-receptor activation in the smooth-muscle cell line DDT1MF-2 stimulates both release of Ca2+ from intracellular stores [inositol 1,4,5-triphosphate (InsP3)-mediated] and Ca2+ influx through a receptor-activated Ca2+ channel. The subsequent refilling of the InsP3-sensitive intracellular Ca2+ store is independent of histamine H1-receptor stimulation (mepyramine-insensitive) and occurs without an observable rise in cytosolic free Ca2+.

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