Abstract
Background: Acute withdrawal symptoms in nicotine user predispose them to relapse during cessation attempts and pose difficulty in treatment of nicotine addiction. The present study was undertaken to explore the behavioral effects of azelnidipine in nicotine withdrawal model of mouse.
Method: Swiss albino mice (either sex; 20-25 g) were administrated with nicotine (3.35 mg/kg; s.c.) three times daily for seven days. Nicotine withdrawal was developed by the cessation of nicotine administration and the abstinence signs (rearing, grooming, head shake, jumping, leg licking and genital licking) were observed for 30 min on ninth day. Azelnidipine was administered (6, 9 and 12 mg/kg; p.o.) for seven days to separate groups of mice from 9th to 15th day of nicotine administration. On 15th day, the behavioral studies were carried out to investigate anxiety, memory and depression like behavior, respectively. Afterwards, brain thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH) levels and catalase activity were estimated.
Results: Nicotine abstinent mice showed marked (p < 0.05) signs of anxiety, impaired memory and depression-like symptoms. Nicotine abstinent mice showed increase (p < 0.05) in TBARS levels, decrease in GSH levels and catalase activity. However, azelnidipine administration not only decreased (p < 0.05) abstinence signs but also improved the behavioral scores of animals. Furthermore, AZD administration caused reduction in TBARS levels and enhancement in GSH levels and catalase activity.
Conclusion: Azelnidipine proves effective in the management of nicotine withdrawal symptoms owing to its calcium channel antagonistic and antioxidant properties.
Keywords: Nicotine withdrawal, azelnidipine, oxidative stress, calcium, antioxidant properties, catalase activity.
Graphical Abstract
Current Psychopharmacology
Title:Calcium Channel Blocker Ameliorates Nicotine Withdrawal Symptoms in Mice
Volume: 7
Author(s): Shikha Aggarwal and Nitin Bansal*
Affiliation:
- Department of Pharmacology, Amar Shaheed Baba Ajit Singh Jujhar Singh Memorial College of Pharmacy, Bela, Ropar,India
Keywords: Nicotine withdrawal, azelnidipine, oxidative stress, calcium, antioxidant properties, catalase activity.
Abstract: Background: Acute withdrawal symptoms in nicotine user predispose them to relapse during cessation attempts and pose difficulty in treatment of nicotine addiction. The present study was undertaken to explore the behavioral effects of azelnidipine in nicotine withdrawal model of mouse.
Method: Swiss albino mice (either sex; 20-25 g) were administrated with nicotine (3.35 mg/kg; s.c.) three times daily for seven days. Nicotine withdrawal was developed by the cessation of nicotine administration and the abstinence signs (rearing, grooming, head shake, jumping, leg licking and genital licking) were observed for 30 min on ninth day. Azelnidipine was administered (6, 9 and 12 mg/kg; p.o.) for seven days to separate groups of mice from 9th to 15th day of nicotine administration. On 15th day, the behavioral studies were carried out to investigate anxiety, memory and depression like behavior, respectively. Afterwards, brain thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH) levels and catalase activity were estimated.
Results: Nicotine abstinent mice showed marked (p < 0.05) signs of anxiety, impaired memory and depression-like symptoms. Nicotine abstinent mice showed increase (p < 0.05) in TBARS levels, decrease in GSH levels and catalase activity. However, azelnidipine administration not only decreased (p < 0.05) abstinence signs but also improved the behavioral scores of animals. Furthermore, AZD administration caused reduction in TBARS levels and enhancement in GSH levels and catalase activity.
Conclusion: Azelnidipine proves effective in the management of nicotine withdrawal symptoms owing to its calcium channel antagonistic and antioxidant properties.
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Cite this article as:
Aggarwal Shikha and Bansal Nitin *, Calcium Channel Blocker Ameliorates Nicotine Withdrawal Symptoms in Mice, Current Psychopharmacology 2018; 7 (2) . https://dx.doi.org/10.2174/2211556007666180403114258
DOI https://dx.doi.org/10.2174/2211556007666180403114258 |
Print ISSN 2211-5560 |
Publisher Name Bentham Science Publisher |
Online ISSN 2211-5579 |
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