Background: Mental health has become one of the thrust areas for research given the complexity of the human mind and paucity of treatment strategies to handle its dysfunction effectively. The mental disorders gain prominence due to the damage they can cause to the individual themselves, the people who are in contact with them and to the society at large. Depression is a mental disorder which is encountered frequently and needs immediate attention. Conventional antidepressants such as selective serotonin reuptake inhibitor and tricyclic antidepressants are used in the management of depression. These drugs have a poor safety profile, take time for therapeutic response and have issues with patient compliance as a concern. Hence, it is postulated that concurrent administration of ketamine with conventional antidepressants would relieve the effects of depression more rapidly, would lower the dose of the later and would be more efficacious. Aims and Objectives: To study the antidepressant effect of coadministration of ketamine with conventional antidepressants in animal models of depression. Materials and Methods: The study was a randomized controlled animal study done on 36 male albino BALB/c mice divided into six groups, namely, Group A distilled water i.p., Group B imipramine 10 mg/kg (i.p.), Group C ketamine 10 mg/kg, Group D escitalopram 5 mg/kg (i.p.), Group E imipramine 10 mg/kg (i.p.) and ketamine 10 mg/kg (i.p.), and Group F escitalopram 5 mg/ kg (i.p.) and ketamine 10 mg/kg (i.p.), respectively. The animal model used was the forced swim test. The reduction in immobility time was taken as the guide for the antidepressant effect. Results: The data were analyzed with the one-way ANOVA test using SPSS version 18. The results showed a significant reduction in immobility time and a statistical significance between the groups (P = 0.017). A post-hoc test showed that all the groups, i.e., B, C, D, E, and F significantly reduced the immobility time in comparison with the control Group A. Conclusion: The above results support the fact that coadministration of ketamine can be a treatment modality for the management of depression with the advantage of quicker onset of action.
Objective: Chronic mild stress is the most valid model in inducing depression in rodents. In this method, rats were subjected to CMS for 6 weeks of stress. Methods: In this method, rodents were subjected to a series of mild stressors for CMS for six weeks in an unpredictable manner. Results: Biochemical and pathological changes were observed. Lycopene treatment at 10 mg/kg and 20 mg/kg could revert these biochemical changes. Histopathological studies showed there is a neuronal loss in CMS and CMS+Vehicle groups. Lycopene treatment reverted this condition. Conclusion: Lycopene treatment might revert this biochemical change by inhibiting a rate-limiting enzyme, HMG-CoA reductase. Histopathology of the brain revealed that rats subjected to chronic mild stress showed a decreased neuronal loss in the hippocampus. Lycopene treatment showed a neuroprotective effect against CMS-induced neuronal loss.
Objective: Liver is the most important organ involved in the biotransformation of drugs and hence also a prime site for drug-induced liver injury (DILI). Among the hepatotoxic drugs, paracetamol which is commonly used is a major offender, leading to about 40% of DILI. N-acetyl cysteine is commonly used to manage paracetamol poisoning. However, it has its own disadvantages. This study has been designed to probe into the possibility of an alternative drug for paracetamol-induced hepatotoxicity. The objective is to study the hepatoprotective effect of melatonin on paracetamol-induced hepatotoxicity in albino rats. Materials and Methods: After prior approval from the IAEC, 36 albino rats were divided into six groups of six each. Each group received distilled water, paracetamol, paracetamol+N-acetyl cysteine, paracetamol+melatonin, and paracetamol+melatonin+N-acetyl cysteine, respectively. The liver function tests and histopathology of the liver of all the groups were compared. One-way ANOVA and post hoc Dunnett’s test were used. Results: Melatonin alone and in combination with N-acetyl cysteine is found to have significant hepatoprotective effect in paracetamol-induced acute liver injury. Conclusion: The main reason for hepatotoxicity is depletion of glutathione which is essential for conjugating the toxic metabolite N acetyl-p- benzoquinonimine (NAPQI) and CYP2E1 is playing the vital role of being the rate limiting enzyme initiating the cascade of events leading to acetaminophen hepatotoxicity. This is postulated to be reversed by melatonin.
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