Asrafi Asifa, Aslam Mohammad, Alkhathami Ali G, Hossain Md Sakib, Rakib Imam Hossen, Al Hasan Md Sakib, Nun Feroz Khan, Amin Md Faisal, Islam Muhammad Torequl
Department of Biochemistry and Molecular Biology, Gopalganj Science and Technology University, Gopalganj, Bangladesh.
Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Khalid University, Abha, Saudi Arabia.
Brain Behav. 2025 Jul;15(7):e70675. doi: 10.1002/brb3.70675.
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.
In the In Vivo study, pentylenetetrazol (PTZ) was administered intraperitoneally (i.p.) at 80 mg/kg to induce convulsions, and the test animals were treated orally with three doses of LQB (1, 5, and 10 mg/kg), with carbamazepine (CBZ) at 80 mg/kg as a standard drug.
The results indicated that LQB at all tested doses significantly (p < 0.05) prolonged seizure latency and decreased convulsion frequency, with the 10 mg/kg dose showing the most significant effects. Furthermore, the combination of LQB (10 mg/kg) and CBZ (80 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 kcal/mol, which was moderate compared to CBZ's BA.
LQB showed potential 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.
L-异槲皮苷(LQB)是一种天然存在的生物活性化合物,具有抗炎、抗氧化、抗癌和抗糖尿病特性。然而,其在惊厥管理中的治疗潜力在很大程度上仍未得到探索。本研究的目的是在体内模型中研究LQB的抗惊厥作用,并通过计算机对接模拟检查其分子相互作用。
在体内研究中,腹腔注射(i.p.)80mg/kg的戊四氮(PTZ)以诱导惊厥,受试动物口服三种剂量的LQB(1、5和10mg/kg),以80mg/kg的卡马西平(CBZ)作为标准药物。
结果表明,所有测试剂量的LQB均显著(p<0.05)延长惊厥潜伏期并降低惊厥频率,其中10mg/kg剂量的效果最为显著。此外,LQB(10mg/kg)和CBZ(80mg/kg)的组合导致抗惊厥活性协同增加。在计算机研究中,分子对接分析表明,LQB和CBZ均与电压门控钠通道(VGSC)相互作用,VGSC是参与惊厥的关键受体,LQB的结合亲和力(BA)为-5.4kcal/mol,与CBZ的BA相比适中。
LQB在PTZ诱导惊厥的动物中显示出潜在的抗惊厥活性,可能是通过阻断钠通道受体。需要进一步研究以阐明其在惊厥治疗中的机制和临床潜力。