kt5720  (Tocris)

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: Effects of neural and cyclic nucleotide pathway inhibitors on tectorigenin-induced relaxation in porcine coronary arteries pre-contracted with 100 nM U46619. ( A ) Tetrodotoxin (TTX, 1 µM) and ω-conotoxin GVIA (CTX, 1 µM) had no significant effect on the relaxation induced by 30 µM tectorigenin ( p > 0.05, n = 4). ( B ) Pretreatment with rolipram (1 µM, a selective phosphodiesterase-4 inhibitor) or vardenafil (1 µM, a selective phosphodiesterase-5 inhibitor) did not significantly alter tectorigenin-induced vasorelaxation ( p > 0.05, n = 4). ( C ) Inhibitors of the nitric oxide and cyclic nucleotide pathways, including Nω-nitro-L-arginine (L-NNA, 100 µM), KT5720 (1 µM, a PKA inhibitor), and KT5823 (1 µM, a PKG inhibitor), also did not significantly affect the relaxant response to tectorigenin ( p > 0.05, n = 4). 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:

Journal: iScience

Article Title: Photoactivated adenylyl cyclase in cortical astrocytes promotes synaptic potentiation and reveals alterations in Huntington’s disease

doi: 10.1016/j.isci.2025.113640

Figure Lengend Snippet: Light activated DdPAC-induced synaptic potentiation (DdPAC-LTP) shares properties of theta burst-induced potentiation (TBS-LTP) (A) Theta-burst stimulation induced LTP in cortical slices. Left panel shows a schematic representation of the experimental setup detailing TBS in layer 4 barrel cortex and recording of evoked field potentials in layer 3/4. Middle panel shows the induction of TBS-LTP in the presence of PKA inhibitor (KT5720), NMDA receptor blockers (5,7 DCK, MK801, and AP5). Right panel summarizes the fEPSP slope effects at 60 min in the different conditions. (B) DdPAC stimulation by 660 nm light increases the slope of evoked fEPSPs. Left panel shows a schematic representation of the experimental setup detailing 660 nm illumination, input stimulation (1 Hz) in layer 4 barrel cortex, and recording of evoked fEPSPs in layer 3/4. Middle panel shows the induction of fEPSP potentiation by 660 nm light and in the presence of PKA inhibitor (KT5720), NMDA receptor blockers (5,7 DCK, MK801, and AP5). Right panel shows a summary of the effects on the fEPSP slope. (C) 660 nm light evoked fEPSP in cortical slices expressing DdPAC in WT, IP 3 R2 −/− and CalEX mice. Left panel shows a schematic representation of the astrocytic characteristics of the mouse lines used for MEA recording. Middle panel shows the induction of fEPSP slope potentiation by 660 nm light in the different mouse lines. Right panel shows a summary of the fEPSP slope potentiation effects. (D) 660 nm light evoked field potentials in cortical slices expressing DdPAC in WT in the presence or absence of 1 Hz input during MEA recordings. Middle panel shows the induction of fEPSP slope potentiation by light. Right panel shows a summary of the fEPSP slope potentiation effects. For A–D, Middle panels show plots of fEPSP slope at experimental time points where symbols are mean ± SEM for experiments in separate slices (n = 4–5), with symbols corresponding to indicated experimental conditions. Panels on the right show summary bar graphs of mean ± SEM (n = 4–5) of normalised fEPSP slope 60 min post stimulation, where each point represents data from a single slice. For comparison between LTP and baseline in MEA recordings, paired Student’s t test was used (∗∗ p < 0.01). Differences between the two independent groups were determined by the Mann-Whitney test (∗ p < 0.05 and ∗∗ p < 0.01).

Article Snippet: PKA inhibitor KT5720 , Hello Bio: https://hellobio.com/kt-5720.html , HB0361.

Techniques: Expressing, Comparison, MANN-WHITNEY

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: Effects of neural and cyclic nucleotide pathway inhibitors on tectorigenin-induced relaxation in porcine coronary arteries pre-contracted with 100 nM U46619. ( A ) Tetrodotoxin (TTX, 1 µM) and ω-conotoxin GVIA (CTX, 1 µM) had no significant effect on the relaxation induced by 30 µM tectorigenin ( p > 0.05, n = 4). ( B ) Pretreatment with rolipram (1 µM, a selective phosphodiesterase-4 inhibitor) or vardenafil (1 µM, a selective phosphodiesterase-5 inhibitor) did not significantly alter tectorigenin-induced vasorelaxation ( p > 0.05, n = 4). ( C ) Inhibitors of the nitric oxide and cyclic nucleotide pathways, including Nω-nitro-L-arginine (L-NNA, 100 µM), KT5720 (1 µM, a PKA inhibitor), and KT5823 (1 µM, a PKG inhibitor), also did not significantly affect the relaxant response to tectorigenin ( p > 0.05, n = 4). 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: