Protective role of cod liver oil on hippocampal oxidative damage and neuronal count in Wistar rat model of comorbid depression.

Background: Proper nutrition and balanced diet have a profound influence on mental well-being. Nutritional psychiatry plays an important role in influencing a healthy mind and body. The animal model of chronic unpredictable stress has been considered the effective model to explore research on anxiety and depression. Aim: The present study aimed to explore the protective role of cod liver oil on various biochemical and neuronal analyses in the hippocampus tissue of the Wistar rat model of comorbid depression. Methods: Healthy adult albino rats of Wistar strain weighing (120-160 g) were divided into control groups and experimental groups. These groups were further categorized into various subgroups based on stress exposure, cod liver oil, and antidepressant treatment. Six animals were taken in each group. The duration of stress exposure was for 15 days. After the experimentation procedure, the animals were anesthetized and hippocampus was dissected for the estimations of various biochemical and neurological parameters. Results: The combination of cod liver oil with the antidepressant significantly (p < 0.001) decreased the lipid peroxidation level. Total antioxidant (TAO) and superoxide dismutase (SOD) levels significantly increased (p < 0.001) in the hippocampus. Treatment of cod liver oil during the stress exposure increased (p < 0.001) the neuronal count. Conclusion: Cod liver oil proved to be an effective antidepressant agent by increasing the antioxidants and promoting neurogenesis in the hippocampus.

Chronic unpredictable stress-induced inflammation and quantitative analysis of neurons of distinct brain regions in Wistar rat model of comorbid depression.

BACKGROUND AND AIM: Depression and anxiety are the most prominent neuropsychiatric disease and have been considered as the most burdensome diseases of society. The hippocampus and prefrontal cortex have a prominent role in stress-induced neurological disorders. Chronic unpredictable stress exposed rats are a perfect model in understanding comorbid depression and anxiety disorders. The inflammatory response occurring in the body has been linked to C-reactive protein (CRP) in many diseased conditions. The present research primarily focus on the possible correlation of Cortisol, CRP level and neuronal assay in different regions of hippocampus, dentate gyrus (DG), and prefrontal cortex. MATERIALS AND METHODS: The control group of rats (n=6) was not exposed to any stress. Whereas, the experimental stress group (n=6) of rats was exposed to various stressors for 15 days. After the experimentation procedures, the blood samples were collected and brain dissection was done. The neurons in the prefrontal cortex, the DG along with various hippocampal regions was counted. Statistical analysis was performed using student's t-test and p<0.05 was expressed as statistically significant. RESULTS: Animals exposed to chronic unpredictable stressors showed a significant (p<0.0001) decrease in the neuronal count in prefrontal cortex and hippocampus. A significant rise in the serum cortisol (p<0.0001) and CRP (p<0.001) was witnessed in the stressed group. CONCLUSION: Our results demonstrate that chronic unpredictable stress exposure has affected neurogenesis in prefrontal cortex and hippocampal regions. Decreased neurogenesis was well in coordinance with the increase in cortisol and CRP. The chronic unpredictable stress-induced inflammatory response correlated to various brain regions might provoke insights into a variety of new drugs targeting neurogenesis.

Evaluation of biomarkers of stress in chronic stress-exposed comorbid depression model Wistar rats.

Background In recent years, increased stress in human life has a dual effect on brain and body physiology. Chronic stress takes a toll on physiology as well as on quality of life, ultimately leading to affective disorders. Rodent models are indispensable tools for studying the etiology and progress of depression. C-reactive protein has been proposed as a novel inflammatory marker. Methods Rats were divided into control and experimental stress groups (n = 6 each). The experimental group consisted of rats that were exposed to a set of chronic unpredictable stressors for 15 days. At the end of the 15th day, the animals were anesthetized, and blood samples were collected through cardiac puncture. Then the blood samples were analyzed for selected biochemical and oxidative stress parameters. Results Serum glutamic oxaloacetic transaminase (p < 0.0001), serum glutamic pyruvic transaminase (p < 0.001), serum malondialdehyde (p < 0.0001), total antioxidant level (p < 0.0001), and serum cortisol (p < 0.0001) were significantly increased in the stressed group when compared with the control group. C-reactive protein significantly (p < 0.0001) increased in the stressed group when compared with the control group. Conclusion Our results demonstrate that chronic unpredictable stress ameliorated depression-like behavior, which might have caused the dysregulation of the hypothalamic-pituitary-adrenal axis, causing the imbalance in the biochemical and oxidative parameters increasing the inflammatory markers. The inflammation-induced model of the chronic unpredictable stress model of comorbid depression might provide a variety of new targets for antidepressant therapies.