<i>Cortex phellodendri</i> Extract Relaxes Airway Smooth Muscle

Jiang, Qiu Ju; Chen, Weiwei; Hong, Dan; Tan, Li; Zhu, He; Yang, Guangzhong; Shen, Jinhua; Peng, Yong; Zhao, Ping; Yu, Meng; Ma, Li-Qun; Tang, Xiao; Wang, Zhuo; Dai, Jiapei; Qin, Gangjian; Zou, Chunbin; Liu, Qing Hua

doi:10.1155/2016/8703239

Cited by 20 publications

(11 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…According to the dose-contraction curve (see supplementary material, Fig. S1B) and the results of our previous studies [39, 44], the effective concentration 100% (EC 100 ) was 80 mM, which could maximally activate Ca 2+ permeable channels; thus, this concentration was applied. As shown in Fig.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Relaxing Effect of TSU-68, an Antiangiogenic Agent, on Mouse Airway Smooth Muscle

Tan

Lei

Lü

et al. 2017

Cell Physiol Biochem

Self Cite

View full text Add to dashboard Cite

Background/Aims: Recently, some small-molecule compounds that were designed for cancer therapy have acquired new roles in the treatment of pulmonary diseases. However, drug screening aimed at abnormal muscle contraction is still limited. TSU-68 is a potent, orally administered, small-molecule agent that can reduce the vascular endothelial growth factor (VEGF)-induced Ca²⁺ increase in endothelial cells. We questioned whether TSU-68 could also affect calcium influx and relax airway smooth muscle (ASM) cells. The current study aimed to investigate these effects and to explore the underlying mechanisms. Methods: The effects of TSU-68 on ASM cells were studied in mice using a series of biophysiological techniques, including force measurement and patch-clamp experiments. Results: TSU-68 inhibited high K⁺ or acetylcholine chloride (ACh)-induced pre-contracted mouse tracheal rings in a concentration-dependent manner. Further research demonstrated that the TSU-68-induced ASM relaxation was mediated by calcium, which was decreased by blocking voltage-dependent Ca²⁺ channels (VDCCs) and non-selective cation channels (NSCCs). Conclusion: Our data indicated that TSU-68 relaxes tense ASM by reducing the intracellular Ca²⁺ concentration through blocking VDCCs and NSCCs, which suggested that this small molecule might be useful in the treatment of abnormal smooth muscle.

show abstract

Section: Resultsmentioning

confidence: 99%

“…To further identify the NSCCs involved in TSU-68-blocked Ca 2+ influx at the molecular level, the TRPC3 inhibitor Pyr3 [44, 53] and gadolinium, which is a blocker of TRPC1, 3, 5, 6, and 7 [54], were applied sequentially. As shown in Fig.…”

Section: Resultsmentioning

confidence: 99%

Relaxing Effect of TSU-68, an Antiangiogenic Agent, on Mouse Airway Smooth Muscle

Tan

Lei

Lü

et al. 2017

Cell Physiol Biochem

Self Cite

View full text Add to dashboard Cite

show abstract

“…Additionally, ASM contraction was indirectly measured in mouse lung slices 25 , 27 . Briefly, after the mice were euthanized, the tracheae and lungs were exposed.…”

Section: Methodsmentioning

confidence: 99%

Polygonum aviculare L. extract and quercetin attenuate contraction in airway smooth muscle

Luo

Lü

et al. 2018

Sci Rep

Self Cite

View full text Add to dashboard Cite

Because of the serious side effects of the currently used bronchodilators, new compounds with similar functions must be developed. We screened several herbs and found that Polygonum aviculare L. contains ingredients that inhibit the precontraction of mouse and human airway smooth muscle (ASM). High K+-induced precontraction in ASM was completely inhibited by nifedipine, a selective blocker of L-type voltage-dependent Ca2+ channels (LVDCCs). However, nifedipine only partially reduced the precontraction induced by acetylcholine chloride (ACH). Additionally, the ACH-induced precontraction was partly reduced by pyrazole-3 (Pyr3), a selective blocker of TRPC3 and stromal interaction molecule (STIM)/Orai channels. These channel-mediated currents were inhibited by the compounds present in P. aviculare extracts, suggesting that this inhibition was mediated by LVDCCs, TRPC3 and/or STIM/Orai channels. Moreover, these channel-mediated currents were inhibited by quercetin, which is present in P. aviculare extracts. Furthermore, quercetin inhibited ACH-induced precontraction in ASM. Overall, our data indicate that the ethyl acetate fraction of P. aviculare and quercetin can inhibit Ca2+-permeant LVDCCs, TRPC3 and STIM/Orai channels, which inhibits the precontraction of ASM. These findings suggest that P. aviculare could be used to develop new bronchodilators to treat obstructive lung diseases such as asthma and chronic obstructive pulmonary disease.

show abstract

“…To further identify the specific components of NSCCs involved in coptisine-blocked Ca 2+ influx, TRPC3 inhibitor Pyr3 [29,30] and gadolinium, which is a blocker of TRPC1, 3, 5, 6 and 7 [31] were employed sequentially. As shown in Figure 6E,F, in the presence of nifedipine, ACh induced a transient contraction under Ca 2+ -free conditions, which indicated that intracellular Ca 2+ was transiently released after the addition of ACh.…”

Section: Coptisine Blocked Ach-evoked Ca 2+ Influxmentioning

confidence: 99%

Coptisine, a protoberberine alkaloid, relaxes mouse airway smooth muscle via blockade of VDLCCs and NSCCs

et al. 2020

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Cortex phellodendri Extract Relaxes Airway Smooth Muscle

Cited by 20 publications

References 25 publications

Relaxing Effect of TSU-68, an Antiangiogenic Agent, on Mouse Airway Smooth Muscle

Relaxing Effect of TSU-68, an Antiangiogenic Agent, on Mouse Airway Smooth Muscle

Polygonum aviculare L. extract and quercetin attenuate contraction in airway smooth muscle

Coptisine, a protoberberine alkaloid, relaxes mouse airway smooth muscle via blockade of VDLCCs and NSCCs

Contact Info

Product

Resources

About