Cannabidiol interactions in the voltage-gated calcium channel by molecular docking: its role in the neuronal inhibitory mechanism

Objective: to analyzer the interactions of cannabidiol in the CaV 3.2 through molecular docking. Methodology: this is a research with in silico approach, which CBD and gabapentin (GBP) were employed as test substances, and CaV 3.2 channel the target protein. Molecular docking experiments were realiz...

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Bibliographic Details
Authors: Arruda, Gisele Evelin de Jesus, Silva Júnior, Gidelson José, Mendes, Nathalia Napoli, Mendes, Gustavo Napoli, Fernandes, Luana Carmélia de Lira, Costa, Alessandra Emertice de Almeida, Silva, Joelmir Lucena Veiga da
Format: article
Status:Published version
Publication Date:2023
Country:Brasil
Institution:Faculdade de Medicina de Olinda (FMO)
Repository:Anais da Faculdade de Medicina de Olinda (Online)
Language:English
OAI Identifier:oai:ojs.afmo.emnuvens.com.br:article/283
Online Access:https://afmo.emnuvens.com.br/afmo/article/view/283
Access Level:Open access
Keyword:Canabidiol
Analgésico
Modelagem de medicamentos
Canal de cálcio dependente de voltagem
Cannabidiol
Analgesic
Drug modeling
Voltage-gated calcium channel
Description
Summary:Objective: to analyzer the interactions of cannabidiol in the CaV 3.2 through molecular docking. Methodology: this is a research with in silico approach, which CBD and gabapentin (GBP) were employed as test substances, and CaV 3.2 channel the target protein. Molecular docking experiments were realized by Dockthor. The drugs simulations were classified in order of highest affinity in the channel. The binding energy scores were linked using Student t-test by GraphPad Prism software, the values were significantly different when p < 0.05. Results: the spatial positions into CBD or GBP and CaV 3.2 were 1.000,000 conformers. Our data showed that the binding energies of CaV 3.2 channel and CBD or GBP were - 6.493 ± 0.07 and - 6.842 ± 0.19 kcal/mol, respectively. Those values did not show statistically difference (p = 0.08), suggesting that both drugs bind similarly the CaV 3.2, however both chemicals connected the distinct sites. Conclusions: CBD binds to CaV 3.2, which corroborates its blockade channel. Those data support the analgesic effect of CBD through the neuronal inhibitory pathway.