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L‐quebrachitol Modulates the Anti‐convulsant Effects of Carbamazepine Possibly Through Voltage‐gated Sodium Channel Blocking Mechanism in Chicks: In Vivo and In Silico Studies

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Udgivet i:Brain and Behavior vol. 15, no. 7 (Jul 1, 2025)
Hovedforfatter: Asrafi, Asifa
Andre forfattere: Aslam, Mohammad, Alkhathami, Ali G., Hossain, Md. Sakib, Rakib, Imam Hossen, Al Hasan, Md. Sakib, Nun, Feroz Khan, Amin, Md. Faisal, Islam, Muhammad Torequl
Udgivet:
John Wiley & Sons, Inc.
Fag:
Bangladesh
Convulsions & seizures
Anticonvulsants
Epilepsy
Animals
Sodium
Free radicals
Natural products
Mutation
Drug dosages
Oxidative stress
Online adgang:Citation/Abstract
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Resumen:ABSTRACT Introduction L‐Quebrachitol (LQB), a naturally occurring bioactive compound, exhibits anti‐inflammatory, anti‐oxidant, anti‐cancer, and anti‐diabetic properties. However, its therapeutic potential in convulsant management remains largely unexplored. The objective of this study was to investigate the anticonvulsant effects of LQB in an In Vivo model and to examine its molecular interactions via In Silico docking simulations. Methods In the In Vivo study, pentylenetetrazol (PTZ) was administered intraperitoneally (i.p.) at 80&#xa0;mg/kg to induce convulsions, and the test animals were treated orally with three doses of LQB (1, 5, and 10&#xa0;mg/kg), with carbamazepine (CBZ) at 80&#xa0;mg/kg as a standard drug. Results The results indicated that LQB at all tested doses significantly (p < 0.05) prolonged seizure latency and decreased convulsion frequency, with the 10&#xa0;mg/kg dose showing the most significant effects. Furthermore, the combination of LQB (10&#xa0;mg/kg) and CBZ (80&#xa0;mg/kg) resulted in a synergistic increase in anticonvulsant activity. In the In Silico study, molecular docking analysis revealed that both LQB and CBZ interacted with the voltage‐gated sodium channel (VGSC), a key receptor involved in convulsions, with LQB demonstrating a binding affinity (BA) of −5.4&#xa0;kcal/mol, which was moderate compared to CBZ's BA. Conclusion LQB showed potential&#xa0;anti‐convulsant activity in PTZ‐induced convulsion animals, possibly through blocking sodium channel receptors. Further studies are needed to clarify its mechanisms and clinical potential in convulsion treatment.
ISSN:2162-3279
DOI:10.1002/brb3.70675
Fuente:Health & Medical Collection