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acetylcholine ach  (MedChemExpress)


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    Structured Review

    MedChemExpress acetylcholine ach
    Adenosine mitigated the neuromuscular blockade caused by B. multicinctus venom. a) The effect of B. multicinctus venom (3 µg/mL) on the inhibition of indirect twitches in chick biventer cervicis (BC) preparations, and the role of adenosine (30 µg/mL) in alleviating neuromuscular blockade; b) Columns representing the effects of B. multicinctus venom (3 µg/mL) and adenosine (30 µg/mL) on responses to exogenous <t>acetylcholine</t> (ACh; 1 mM), carbachol (CCh; 20 µM) and potassium chloride (KCl; 40 mM) in BC preparations; c) The effect of B. multicinctus venom (3 µg/mL) on the inhibition of indirect twitches in mouse phrenic nerve-diaphragm (PND) preparations, and the role of adenosine (30 µg/mL) in alleviating neuromuscular blockade; d) Columns representing the effects of B. multicinctus venom (3 µg/mL) and adenosine (30 µg/mL) on responses to exogenous ACh (1 mM), CCh (20 μM), and KCl (40 mM) in PND preparations. The points in a/c and the columns in b/d represent the mean ± standard error of mean (n = 3 for each group); * P < 0.05, significantly different from the venom-only group. ADO refers to adenosine .
    Acetylcholine Ach, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 22 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Preclinical evidence of adenosine for early intervention in Bungarus multicinctus envenomation"

    Article Title: Preclinical evidence of adenosine for early intervention in Bungarus multicinctus envenomation

    Journal: Journal of Advanced Research

    doi: 10.1016/j.jare.2025.06.012

    Adenosine mitigated the neuromuscular blockade caused by B. multicinctus venom. a) The effect of B. multicinctus venom (3 µg/mL) on the inhibition of indirect twitches in chick biventer cervicis (BC) preparations, and the role of adenosine (30 µg/mL) in alleviating neuromuscular blockade; b) Columns representing the effects of B. multicinctus venom (3 µg/mL) and adenosine (30 µg/mL) on responses to exogenous acetylcholine (ACh; 1 mM), carbachol (CCh; 20 µM) and potassium chloride (KCl; 40 mM) in BC preparations; c) The effect of B. multicinctus venom (3 µg/mL) on the inhibition of indirect twitches in mouse phrenic nerve-diaphragm (PND) preparations, and the role of adenosine (30 µg/mL) in alleviating neuromuscular blockade; d) Columns representing the effects of B. multicinctus venom (3 µg/mL) and adenosine (30 µg/mL) on responses to exogenous ACh (1 mM), CCh (20 μM), and KCl (40 mM) in PND preparations. The points in a/c and the columns in b/d represent the mean ± standard error of mean (n = 3 for each group); * P < 0.05, significantly different from the venom-only group. ADO refers to adenosine .
    Figure Legend Snippet: Adenosine mitigated the neuromuscular blockade caused by B. multicinctus venom. a) The effect of B. multicinctus venom (3 µg/mL) on the inhibition of indirect twitches in chick biventer cervicis (BC) preparations, and the role of adenosine (30 µg/mL) in alleviating neuromuscular blockade; b) Columns representing the effects of B. multicinctus venom (3 µg/mL) and adenosine (30 µg/mL) on responses to exogenous acetylcholine (ACh; 1 mM), carbachol (CCh; 20 µM) and potassium chloride (KCl; 40 mM) in BC preparations; c) The effect of B. multicinctus venom (3 µg/mL) on the inhibition of indirect twitches in mouse phrenic nerve-diaphragm (PND) preparations, and the role of adenosine (30 µg/mL) in alleviating neuromuscular blockade; d) Columns representing the effects of B. multicinctus venom (3 µg/mL) and adenosine (30 µg/mL) on responses to exogenous ACh (1 mM), CCh (20 μM), and KCl (40 mM) in PND preparations. The points in a/c and the columns in b/d represent the mean ± standard error of mean (n = 3 for each group); * P < 0.05, significantly different from the venom-only group. ADO refers to adenosine .

    Techniques Used: Inhibition

    Adenosine mitigates Bungarus multicinctus venom-induced muscle and membrane damage, as well as neuromuscular blockade. (a) Serum levels of ALP, CK, LDH, ALT, and AST were quantified in PBS control (grey), venom only (yellow), and venom-plus-adenosine (blue) groups. (b) Diaphragm sections from PBS control, venom-only, and venom-plus-adenosine groups were incubated with FITC-conjugated α-bungarotoxin antibody and imaged. Green fluorescence indicates the distribution of nAChR channels at neuromuscular junctions. Scale bars: 50 µm. (c) Quantification of intracellular fluorescence intensity in Diaphragm sections from PBS control (grey), venom-only (yellow), and venom-plus-adenosine (blue) groups. All data in (a and c) represent mean ± SEM (n = 5 for each group). ****P < 0.0001, ***P < 0.001, **P < 0.01, *P < 0.05, ns: not significant (one-way ANOVA followed by Tukey’s post hoc test). Abbreviations: AST – Aspartate Aminotransferase, ALT – Alanine Aminotransferase, Cr – Creatinine, ALP – Alkaline Phosphatase, CK – Creatine Kinase, LDH – Lactate Dehydrogenase. nAChR-nicotinic acetylcholine receptor. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
    Figure Legend Snippet: Adenosine mitigates Bungarus multicinctus venom-induced muscle and membrane damage, as well as neuromuscular blockade. (a) Serum levels of ALP, CK, LDH, ALT, and AST were quantified in PBS control (grey), venom only (yellow), and venom-plus-adenosine (blue) groups. (b) Diaphragm sections from PBS control, venom-only, and venom-plus-adenosine groups were incubated with FITC-conjugated α-bungarotoxin antibody and imaged. Green fluorescence indicates the distribution of nAChR channels at neuromuscular junctions. Scale bars: 50 µm. (c) Quantification of intracellular fluorescence intensity in Diaphragm sections from PBS control (grey), venom-only (yellow), and venom-plus-adenosine (blue) groups. All data in (a and c) represent mean ± SEM (n = 5 for each group). ****P < 0.0001, ***P < 0.001, **P < 0.01, *P < 0.05, ns: not significant (one-way ANOVA followed by Tukey’s post hoc test). Abbreviations: AST – Aspartate Aminotransferase, ALT – Alanine Aminotransferase, Cr – Creatinine, ALP – Alkaline Phosphatase, CK – Creatine Kinase, LDH – Lactate Dehydrogenase. nAChR-nicotinic acetylcholine receptor. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Techniques Used: Membrane, Control, Incubation, Fluorescence



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    Image Search Results


    Adenosine mitigated the neuromuscular blockade caused by B. multicinctus venom. a) The effect of B. multicinctus venom (3 µg/mL) on the inhibition of indirect twitches in chick biventer cervicis (BC) preparations, and the role of adenosine (30 µg/mL) in alleviating neuromuscular blockade; b) Columns representing the effects of B. multicinctus venom (3 µg/mL) and adenosine (30 µg/mL) on responses to exogenous acetylcholine (ACh; 1 mM), carbachol (CCh; 20 µM) and potassium chloride (KCl; 40 mM) in BC preparations; c) The effect of B. multicinctus venom (3 µg/mL) on the inhibition of indirect twitches in mouse phrenic nerve-diaphragm (PND) preparations, and the role of adenosine (30 µg/mL) in alleviating neuromuscular blockade; d) Columns representing the effects of B. multicinctus venom (3 µg/mL) and adenosine (30 µg/mL) on responses to exogenous ACh (1 mM), CCh (20 μM), and KCl (40 mM) in PND preparations. The points in a/c and the columns in b/d represent the mean ± standard error of mean (n = 3 for each group); * P < 0.05, significantly different from the venom-only group. ADO refers to adenosine .

    Journal: Journal of Advanced Research

    Article Title: Preclinical evidence of adenosine for early intervention in Bungarus multicinctus envenomation

    doi: 10.1016/j.jare.2025.06.012

    Figure Lengend Snippet: Adenosine mitigated the neuromuscular blockade caused by B. multicinctus venom. a) The effect of B. multicinctus venom (3 µg/mL) on the inhibition of indirect twitches in chick biventer cervicis (BC) preparations, and the role of adenosine (30 µg/mL) in alleviating neuromuscular blockade; b) Columns representing the effects of B. multicinctus venom (3 µg/mL) and adenosine (30 µg/mL) on responses to exogenous acetylcholine (ACh; 1 mM), carbachol (CCh; 20 µM) and potassium chloride (KCl; 40 mM) in BC preparations; c) The effect of B. multicinctus venom (3 µg/mL) on the inhibition of indirect twitches in mouse phrenic nerve-diaphragm (PND) preparations, and the role of adenosine (30 µg/mL) in alleviating neuromuscular blockade; d) Columns representing the effects of B. multicinctus venom (3 µg/mL) and adenosine (30 µg/mL) on responses to exogenous ACh (1 mM), CCh (20 μM), and KCl (40 mM) in PND preparations. The points in a/c and the columns in b/d represent the mean ± standard error of mean (n = 3 for each group); * P < 0.05, significantly different from the venom-only group. ADO refers to adenosine .

    Article Snippet: Acetylcholine (ACh), d-tubocurarine chloride (dTC), KCl, and chlorogenic acid were acquired from Sigma-Aldrich Chemical Co. (St. Louis, MO, USA), and carbamylcholine (CCh) was purchased from MedChem Express Co., Ltd. (Monmouth Junction, NJ, USA).

    Techniques: Inhibition

    Adenosine mitigates Bungarus multicinctus venom-induced muscle and membrane damage, as well as neuromuscular blockade. (a) Serum levels of ALP, CK, LDH, ALT, and AST were quantified in PBS control (grey), venom only (yellow), and venom-plus-adenosine (blue) groups. (b) Diaphragm sections from PBS control, venom-only, and venom-plus-adenosine groups were incubated with FITC-conjugated α-bungarotoxin antibody and imaged. Green fluorescence indicates the distribution of nAChR channels at neuromuscular junctions. Scale bars: 50 µm. (c) Quantification of intracellular fluorescence intensity in Diaphragm sections from PBS control (grey), venom-only (yellow), and venom-plus-adenosine (blue) groups. All data in (a and c) represent mean ± SEM (n = 5 for each group). ****P < 0.0001, ***P < 0.001, **P < 0.01, *P < 0.05, ns: not significant (one-way ANOVA followed by Tukey’s post hoc test). Abbreviations: AST – Aspartate Aminotransferase, ALT – Alanine Aminotransferase, Cr – Creatinine, ALP – Alkaline Phosphatase, CK – Creatine Kinase, LDH – Lactate Dehydrogenase. nAChR-nicotinic acetylcholine receptor. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Journal: Journal of Advanced Research

    Article Title: Preclinical evidence of adenosine for early intervention in Bungarus multicinctus envenomation

    doi: 10.1016/j.jare.2025.06.012

    Figure Lengend Snippet: Adenosine mitigates Bungarus multicinctus venom-induced muscle and membrane damage, as well as neuromuscular blockade. (a) Serum levels of ALP, CK, LDH, ALT, and AST were quantified in PBS control (grey), venom only (yellow), and venom-plus-adenosine (blue) groups. (b) Diaphragm sections from PBS control, venom-only, and venom-plus-adenosine groups were incubated with FITC-conjugated α-bungarotoxin antibody and imaged. Green fluorescence indicates the distribution of nAChR channels at neuromuscular junctions. Scale bars: 50 µm. (c) Quantification of intracellular fluorescence intensity in Diaphragm sections from PBS control (grey), venom-only (yellow), and venom-plus-adenosine (blue) groups. All data in (a and c) represent mean ± SEM (n = 5 for each group). ****P < 0.0001, ***P < 0.001, **P < 0.01, *P < 0.05, ns: not significant (one-way ANOVA followed by Tukey’s post hoc test). Abbreviations: AST – Aspartate Aminotransferase, ALT – Alanine Aminotransferase, Cr – Creatinine, ALP – Alkaline Phosphatase, CK – Creatine Kinase, LDH – Lactate Dehydrogenase. nAChR-nicotinic acetylcholine receptor. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Article Snippet: Acetylcholine (ACh), d-tubocurarine chloride (dTC), KCl, and chlorogenic acid were acquired from Sigma-Aldrich Chemical Co. (St. Louis, MO, USA), and carbamylcholine (CCh) was purchased from MedChem Express Co., Ltd. (Monmouth Junction, NJ, USA).

    Techniques: Membrane, Control, Incubation, Fluorescence