Catechin is an active ingredient of green tea. It is reported to inhibit corticosteroid-induced anxiety and depression-like symptoms. Considering the complex nature of depression, effects of catechin need to be studied in a clinically relevant depression model. The present study was designed to explore the antidepressant effect of catechin in Sprague Dawley rats subjected to chronic unpredictable mild stress (CUMS). Animals were subjected to CUMS and treated with (+)-catechin (50 mg/kg) or escitalopram (10 mg/kg) orally; a CUMS control and a vehicle control that was not exposed to CUMS were also established. Various stressors were applied daily in an unpredictable manner for 8 weeks achieve CUMS. Sucrose preference test were performed after 4 and 8 weeks and forced swim tests (FSTs) were conducted at weeks 4, 6 and 8. At the end of week 8, animals were sacrificed and the brain homogenate was studied for antioxidant parameters. Compared with the vehicle control, animals of the CUMS control group showed a significant decrease in sucrose intake. Catechin and escitalopram treatment significantly improved the sucrose intake compared with the CUMS control. A similar trend was observed in the FSTs, where catechin and escitalopram treatment significantly reduced the immobility time, and antioxidant parameters, including catalase, glutathione and superoxide dismutase levels were recovered in treated animals compared with the CUMS control. Thus, it was concluded that catechin reverses CUMS-induced depression in rats by ameliorating oxidative stress, which may help to develop a novel treatment for major depressive disorder.

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It is well established that chronic exposure to stressful events plays an important role in the etiology of depression. Saraca asoca (Roxb.), De. wild, or Saraca indica, belonging to family Fabaceae, is endogenous to India. The flowers, seeds, bark, and leaves of the plant have been used widely in Ayurveda medicine. The bark extract of S. asoca has shown chemoprotection, myeloprotection, and antioxidant potential. Owing to the above-mentioned properties of the plant, the present study sought to evaluate the effect of a methanolic extract of S. asoca bark in rats exposed to chronic unpredictable mild stress (CUMS) daily for 8 weeks using a forced-swim test, an open-field test, and a sucrose-preference test. The effect of the extract on endogenous antioxidant levels in the brain was also assessed using catalase activity, superoxide dismutase activity, reduced glutathione levels, and malondialdehyde levels in the brain. Male Sprague-Dawley rats received 100 mg/kg (oral) of the extract daily 1 h before daily stress exposure for 8 weeks. The extract showed a significant reduction in the immobility time in the forced-swim test, increased the total number of line crossing, rearing, and grooming in the open-field test, and increased the sucrose consumption as well as the levels of endogenous antioxidants significantly in comparison with the CUMS control group. Therefore, S. asoca might be a useful agent for the treatment or alleviation of symptoms associated with depression possibly by reducing CUMS-induced oxidative stress and reactive oxygen species in the brain.

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Chitosan, the deacetylated form of chitin, a natural polysaccharide, is known for its various biomedical applications. The present study aimed at exploring the immunomodulatory properties of chitosan (CSNP) and gallic acid‐grafted chitosan (cGANP) nanoparticles in mice model of cyclophosphamide (CPA)‐induced immunosuppression. In addition, chitooligosaccharides, the hydrolysed form of chitin and chitosan, were also evaluated for its potential against immunosuppression in mice. CPA (80 mg/kg/ip) induced significant immunosuppression, which was reversed with cGANP treatment as indicated by a significant increase in the thymus and spleen indices compared to the CPA‐treated group. The CSNP and chitooligosaccharides (chitin and chitosan) failed to reverse CPA‐induced changes. ELISA revealed an elevation in the levels of IL‐6 and a reduction in IFN‐γ levels with CPA treatment. All the test compounds reduced the IL‐6 levels, whereas only the nanoparticle formulations (CSNP and cGANP) exhibited a significant augmentation in the IFN‐γ levels. Both the cytokines, IL‐6 and IFN‐γ, are secreted separately by two different types of T helper cells (Th cells), which mediate cellular and humoral immune responses in a coordinated manner. Th‐1 cells release IFN‐γ, facilitating cell‐mediated immunity, whereas IL‐6 is released by Th‐2 cells, expediting humoral immune response. The nanoparticles (CSNP and cGANP) seemed to be better immune enhancers than the chitooligosaccharides owing to their ability to reverse the cytokine changes induced by CPA. Overall, it was evident that the nanoparticles, most likely, boosted the cell‐mediated immunity through the induction of the Th‐1 branch of the immune response.

Rationale Chemotherapy-induced cognitive impairment (CICI), chemobrain, and chemofog are the common terms for mental dysfunction in a cancer patient/survivor under the influence of chemotherapeutics. CICI is manifested as short/long term memory problems and delayed mental processing, which interferes with a person’s day-to-day activities. Understanding CICI mechanisms help in developing therapeutic interventions that may alleviate the disease condition. Animal models facilitate critical evaluation to elucidate the underlying mechanisms and form an integral part of verifying different treatment hypotheses and strategies. Objectives A methodical evaluation of scientific literature is required to understand cognitive changes associated with the use of chemotherapeutic agents in different preclinical studies. This review mainly emphasizes animal models developed with various chemotherapeutic agents individually and in combination, with their proposed mechanisms contributing to the cognitive dysfunction. This review also points toward the analysis of chemobrain in healthy animals to understand the mechanism of interventions in absence of tumor and in tumor-bearing animals to mimic human cancer conditions to screen potential drug candidates against chemobrain. Results Substantial memory deficit as a result of commonly used chemotherapeutic agents was evidenced in healthy and tumor-bearing animals. Spatial and episodic cognitive impairments, alterations in neurotrophins, oxidative and inflammatory markers, and changes in long-term potentiation were commonly observed changes in different animal models irrespective of the chemotherapeutic agent. Conclusion Dyscognition exists as one of the serious side effects of cancer chemotherapy. Due to differing mechanisms of chemotherapeutic agents with differing tendencies to alter behavioral and biochemical parameters, chemotherapy may present a significant risk in resulting memory impairments in healthy as well as tumor-bearing animals.