da Silva Oliveira George L, da Silva José C Correia L, Dos Santos C L da Silva Ana P, Feitosa Chistiane M, de Castro Almeida Fernanda R
Department of Biology, Federal Institute of Mato Grosso, Guaranta do Norte - MT, 78520-000, Guaranta do Norte Campus, Brazil.
Department of Computer Science, Federal University of Piaui, Teresina, 64049-550, Piaui, Brazil.
Curr Mol Pharmacol. 2021;14(1):36-51. doi: 10.2174/1874467213666200510004622.
Central nervous system disorders such as anxiety, depression and epilepsy are characterized by sharing several molecular mechanisms in common and the involvement of the L-arginine/NO pathway in neurobehavioral studies with β-caryophyllene is still little discussed.
One of the objectives of the present study was to demonstrate the anxiolytic behavioral effect of β-caryophyllene (β-CBP) in female Swiss mice, as well as to investigate the molecular mechanisms underlying the results obtained.
This study evaluated the neurobehavioral effects of β-CBP using the open field test, rota- rod test, elevated plus maze test, novelty suppressed feeding test, tail suspension test and forced swim test, as well as pilocarpine, pentylenetetrazole and isoniazid-induced epileptic seizure models.
The results demonstrated that the neuropharmacological activities of β-CBP may involve benzodiazepine/GABAergic receptors, since the pre-treatment of β-CBP (200 mg/kg) associated with flumazenil (5 mg/kg, benzodiazepine receptor antagonist) and bicuculline (1 mg/kg, selective GABAA receptor antagonist) reestablished the anxiety parameters in the elevated plus-maze test, as well as the results of reduced latency to consume food in the novelty suppressed feeding test. In addition to benzodiazepine/GABAergic receptors, the neuropharmacological properties of β-CBP may be related to inhibition of nitric oxide synthesis, since pre-treatment with L-arginine (500-750 mg/kg) reversed significantly the anxiolytic, antidepressant and anticonvulsant activities of β-CBP.
The results obtained provide additional support in understanding the neuromolecular mechanisms underlying the anxiolytic, antidepressant and anticonvulsive properties of β-CBP in female Swiss mice.
焦虑、抑郁和癫痫等中枢神经系统疾病具有一些共同的分子机制，而在神经行为学研究中，β-石竹烯对L-精氨酸/一氧化氮途径的影响仍鲜少被讨论。
本研究的目的之一是证明β-石竹烯（β-CBP）对雌性瑞士小鼠的抗焦虑行为作用，并探究其背后的分子机制。
本研究使用旷场试验、转棒试验、高架十字迷宫试验、新奇抑制摄食试验、悬尾试验和强迫游泳试验，以及毛果芸香碱、戊四氮和异烟肼诱导的癫痫发作模型，评估β-CBP的神经行为学效应。
结果表明，β-CBP的神经药理学活性可能涉及苯二氮䓬/GABA能受体，因为β-CBP（200mg/kg）与氟马西尼（5mg/kg，苯二氮䓬受体拮抗剂）和荷包牡丹碱（1mg/kg，选择性GABAA受体拮抗剂）预处理后，在高架十字迷宫试验中恢复了焦虑参数，以及在新奇抑制摄食试验中缩短了进食潜伏期。除了苯二氮䓬/GABA能受体外，β-CBP的神经药理学特性可能与一氧化氮合成的抑制有关，因为L-精氨酸（500-750mg/kg）预处理显著逆转了β-CBP的抗焦虑、抗抑郁和抗惊厥活性。
所得结果为理解β-CBP对雌性瑞士小鼠抗焦虑、抗抑郁和抗惊厥特性的神经分子机制提供了更多支持。
