Background: The present study aims to assess the effect of vitamin B (Vit B) on depression-like behavior caused by nicotine (Nic) withdrawal, which is more likely due to the anxiogenic effect of Nic in adolescent male rats, through assessing behavioral and biochemical analysis.

Methods: Adolescent male rats were divided into vehicle (received normal saline), and experimental groups that received Nic (2 mg/kg, intraperitoneally (i.p.)) for three consecutive weeks and after that, the group that received normal saline was divided into two groups, one of which returned to a regular diet, and the second one received Vit B (1.5 mg/kg). The Nic group was divided into five groups, one of which received bupropion (Bup, 20 mg/kg), three of which received different doses of Vit B (0.5, 1, and 1.5 mg/kg), and the last one returned to a normal diet without treatment, which was considered as the withdrawal period.

Results: Behavioral analysis showed that Nic withdrawal induced anxiety and depression. Vit B and Bup reduced anxiety and depression induced by Nic withdrawal. The biochemical analysis demonstrated the more activity of oxidative stress factors and pro-inflammatory cytokines in which Nic was administered, whereas both Vit B and Bup reversed the results and improved the activity of both antioxidant and anti-inflammatory parameters. Furthermore, both serum and cortical Vit B levels dramatically decreased in nicotine group, whereas treatment with both Vit B and Bup as desirable treatments corrected Vit B levels.

Conclusion: According to the present findings, the results revealed that Vit B is comparable with Bup in attenuation of Nic withdrawal symptoms. In addition, both Bup and Vit B improved the decreased serum and cortical levels of Vit B, which caused by nicotine. Administration of Vit B in normal animals demonstrated better results in reducing antioxidant and anti-inflammatory parameters, which explores new hope to introduce Vit B as a novel antioxidant and anti-inflammatory agent to treat not only withdrawal, but also other diseases related to the prominent role of oxidative stress or inflammatory pathways, such as Alzheimer's disease.

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http://dx.doi.org/10.1016/j.bcp.2023.115832DOI Listing

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