ibtx  (Alomone Labs)

Journal: Scientific Reports

Article Title: Tectorigenin induces vasorelaxation in porcine coronary arteries through activation of Kv channels and oestrogen receptor modulation

doi: 10.1038/s41598-025-20988-6

Figure Lengend Snippet: Involvement of potassium channels in tectorigenin-induced vasorelaxation in porcine coronary arteries. ( A ) Effects of various potassium channel blockers on vasorelaxation induced by 30 µM tectorigenin. Pretreatment with glibenclamide (10 µM), iberiotoxin (IbTX, 200 nM), tetraethylammonium (TEA, 1 mM), apamin (100 nM), or charybdotoxin (1 µM) did not significantly affect the relaxant response ( p > 0.05), whereas 4-aminopyridine (4-AP, 1 mM) significantly attenuated tectorigenin-induced relaxation ( p < 0.05). ( B ) Concentration-dependent inhibitory effect of 4-AP (1 mM) on tectorigenin-induced relaxation. Significant inhibition was observed at 10 and 30 µM († p < 0.05 vs. corresponding tectorigenin alone), but not at 100 µM. ( C ) Comparison of the relaxant effects of 30 µM tectorigenin in porcine coronary arteries pre-contracted with either 100 nM U46619 or 80 mM KCl. Tectorigenin elicited significant vasorelaxation in U46619-pre-contracted rings but had negligible effect in KCl-contracted rings. Data are expressed as mean ± standard error of the mean (SEM) from four independent hearts. U46619 plateau (normalised to 60 mM KCl) was similar across groups ( p > 0.05; Supplementary Table 2).

Article Snippet: For experimental assays, a range of pharmacological agents was utilised, including U46619, apamin, KT5720, KT5823, and L-NNA (Sigma-Aldrich, MO, USA); rolipram, vardenafil, and TEA (Santa Cruz Biotechnology, CA, USA); IbTX (Alomone Labs, Jerusalem, Israel); glibenclamide (Research Biochemicals International, MA, USA); TTX and 4-AP (Tocris Bioscience, Bristol, UK); CTX (Bachem, Bubendorf, Switzerland); and charybdotoxin, methyl-piperidino-pyrazole (MPP), and PHTPP (Cayman Chemical, MI, USA).

Techniques: Concentration Assay, Inhibition, Comparison

Journal: bioRxiv

Article Title: Natural xanthones as α-Mangostin induce vasorelaxation via binding to key gating residues in the S6 domain of BK channels

doi: 10.1101/2025.10.02.680041

Figure Lengend Snippet: (A) Representative whole-cell current traces of BKα/β1 channels alone and BKα/β1 coexpressed with Ca v 1.2 channels before and after application of 10 µM α-Mangostin. Currents were measured in Ca i 2+ -free conditions in a physiological potassium gradient with a family of voltage steps from -50 mV to +50 mV in 10 mV increments. The inset shows voltage activation with a family protocol up to +200 mV to show the presence of BKα/β1 channels. (B) Currents of BKα/β1 channels and BKα/β1 – Ca v complexes before and after application of 10 µM α-Mangostin plotted against voltage. The last panel shows the α-Mangostin-activated currents for the range -50 to 10 mV obtained by subtracting the current before α-Mangostin application from the current after application for each potential (mean ± SEM, n=8-11 for each condition). (C) Representative contraction force recordings of aortic preparations from mice. 10 µM α-Mangostin were either applied directly to aortic preparations precontracted with 100 nM Noradrenaline (NA; top), or the precontracted preparations were incubated with 100 nM Iberiotoxin (IbTx) before α-Mangostin application and the contraction force was analyzed 10 min after α-Mangostin addition (dotted lines in recordings). The bar graph shows the normalized contraction force of preparations as mean ± SEM together with the median (orange). Data and statistics see Table S13.

Article Snippet: BC5 (Arg-4-methoxy-2-naphthylamine) was obtained from MP Biomedicals (Irvine, USA), and Iberiotoxin from Alomone Labs (Jerusalem, Israel).

Techniques: Activation Assay, Incubation

Journal: Frontiers in Pharmacology

Article Title: Bitter taste receptor agonists induce vasorelaxation in porcine coronary arteries

doi: 10.3389/fphar.2025.1578913

Figure Lengend Snippet: Inhibition of various agents on vasorelaxation induced by flufenamic acid in segments of the porcine coronary artery precontracted with 100 nM U46619. (A) The presence of tetrodotoxin (TTX) did not significantly alter the vasorelaxant action of flufenamic acid. (B) The addition of rolipram and vardenafil also did not significantly modify the vasorelaxation induced by flufenamic acid. (C) Neither KT5720 nor KT5823 significantly affected the vasorelaxant response to flufenamic acid, whereas NG-nitro-L-arginine (L-NNA) significantly inhibited the flufenamic acid-induced vasorelaxation. (D) Iberiotoxin (IbTX) and tetraethylammonium (TEA) had no significant impact on the relaxation response to flufenamic acid, but apamin and glibenclamide significantly decreased the relaxation effect. Error bars represent the standard error of the mean (SEM). The single asterisk (*) denotes a statistically significant deviation from the relaxation effect at 30 μM flufenamic acid, with p < 0.05.

Article Snippet: Additional agents included rolipram, vardenafil, and tetraethylammonium (TEA) from Santa Cruz Biotechnology (Santa Cruz, CA, United States), iberiotoxin (IbTX) from Alomone Labs (Jerusalem, Israel), glibenclamide from Research Biochemicals International (Natick, MA, United States), and tetrodotoxin (TTX) from Tocris Bioscience (Bristol, United Kingdom).

Techniques: Inhibition