Biochemical Alterations In Mice Research Articles

Investigation of Memory Enhancing Activity of Combination Extracts of Bauhinia variegata and Madhuca longifolia Leaves against Colchicine: An Experimental Study and Biochemical Alterations in Mice

Investigation of Memory Enhancing Activity of Combination Extracts of Bauhinia variegata and Madhuca longifolia Leaves against Colchicine: An Experimental Study and Biochemical Alterations in Mice

Dillenia indica fruit extract alleviates sucrose-induced fatty liver and improves serum biochemical alterations in mice

Dillenia indica fruit extract alleviates sucrose-induced fatty liver and improves serum biochemical alterations in mice

Aggressive-like behaviour and neurocognitive impairment in alcohol herbal mixture-fed mice are associated with increased neuroinflammation and neuronal apoptosis in the prefrontal cortex.

Alcohol-induced aggression and related violence is a serious and common social problem globally. Alcohol use is increasingly found in the form of alcoholic herbal mixtures (AHM) with indiscriminate and unregulated alcohol content. This study investigated the effects of AHM on aggressive-like, neurocognitive impairment and brain biochemical alteration in mice. Thirty-two male resident mice were paired housed with female mice for 21 days in four groups (n = 8). Resident mice were treated orally with normal saline, AHM, ethanol and AHM + ethanol daily for 14 days. Aggressive-like behaviour was scored based on the latency and frequency of attacks by the resident mouse on the intruder. Neurocognitive impairment was determined using the Y-maze test (YMT) and novel object recognition test (NORT). Acetylcholinesterase, glutamic acid decarboxylase (GAD), pro-inflammatory and oxidative stress parameters were determined in the prefrontal cortex (PFC). Neuronal morphology, cytochrome c (Cyt-c) and nuclear factor-kappa B (NF-ĸB) expressions were determined. AHM and in combination with ethanol showed an increased index of aggression typified by frequency of attack and reduced latency to attack when compared to normal saline-treated animals. Co-administration of AHM and ethanol significantly reduced cognitive correct alternation (%) and discrimination index in the YMT and NORT, respectively. AHM and ethanol increased acetylcholinesterase, Pro-inflammatory cytokines and oxidative stress parameters while they reduced GAD. There were significantly reduced neuronal counts and increased expression of Cyt-c and NF-ĸB, respectively Alcoholic herbal mixture increased aggressiveness and caused neurocognitive impairment via increased oxido-inflammatory stress in the prefrontal cortex.

Investigation of Memory Enhancing Activity of Madhuca longifolia Leaf Extract against Colchicine: An Experimental Study and Biochemical Alterations in Mice

Investigation of Memory Enhancing Activity of Madhuca longifolia Leaf Extract against Colchicine: An Experimental Study and Biochemical Alterations in Mice

Neuroprotective Effect of Bauhinia variegata Leaf Extract against Colchicine: An Experimental Study on Cognitive Dysfunction and Biochemical Alterations in Mice

Neuroprotective Effect of Bauhinia variegata Leaf Extract against Colchicine: An Experimental Study on Cognitive Dysfunction and Biochemical Alterations in Mice

Selanylimidazopyridine abolishes inflammation- and stress-induced depressive-like behaviors by modulating the oxido-nitrosative system

The 3-[(4-methoxyphenyl)selanyl]-2-phenylimidazo[1,2-a] pyridine (MPI), a novel organic selenium compound, has been receiving increased attention due to its antioxidant effects and its ability to protect against depression-like behaviours. However, it remains elusive whether MPI is able to reverse depressive-like symptoms and biochemical alterations in mice. In the present work, we explored the ability of MPI (10 mg/kg, i.g.) to reverse inflammation- and stress-induced depression-like behaviours in mice injected with tumour necrosis factor (TNF-α) or submitted to acute restraint stress. Depression-like behaviours were evaluated by the tail suspension and splash test and the open field test was used to evaluate the locomotor activity of mice. The prefrontal cortex and hippocampus of mice were used for the evaluation of parameters of oxidonitrosative stress. Here, we showed that a single administration of MPI abolished the depressive-like behaviours induced by TNF-α and acute restraint stress. The oxidative and nitrosative stress presented in mice with depression-like behaviours were also decreased by MPI in the prefrontal cortex and hippocampus. Our findings suggest that MPI presents antidepressant-like activity which is associated with the biochemical regulation of oxidative stress in prefrontal cortex and hippocampus of mice, arising as a promising strategy for the management of depressive symptoms.

In vivo effects of exposure to Golden trumpet Handroanthus chrysotrichus in mice.

The Golden trumpet Handroanthus chrysotrichus is a tree that presents beneficial health properties against various diseases. Thus, this study aims to verify the toxicity of H. chrysotrichus bark extract, observing the effects of exposure to this extract in mice. For this, mice were separated in groups: saline (sterile solution .9%); H. chrysotrichus crude extract (HCCE) 10; HCCE 50, and HCCE 100mg. kg-1 (p.o.). We analyzed HCCE effects on acute (single exposure) and subchronic protocol (14 days exposure). After both exposures, acute, and subchronic, we collected samples from blood, brain, liver, and kidney tissues for biochemical evaluation. In addition, after subchronic exposure, we performed behavioral tests. Acute exposure caused an increase of lipid peroxidation in liver tissue. Moreover, we observed a significant carbonyl increase in liver and brain tissues from HCCE 50mg. kg-1. Kidneys presented carbonyl increase in mice treated with the highest concentration. Besides, creatinine increased in the group of the acute exposure at HCCE 100mg. kg-1. Total leukocyte count decreased in all concentrations tested. Sub-chronic exposure at HCCE 100mg. kg-1 caused a decrease in the number of crossing and an increase in its self-grooming frequency in the open field test. In this exposure, the brain and liver had a significant increase in carbonyl levels in all concentrations. We concluded that H. chrysotrichus cause behavioral and biochemical alterations in mice. HCCE primary targets seem to be the liver, kidneys, and white cells.

The lethality, histological, haematological and biochemical alterations in mice envenomated with Aegaeobuthus nigrocinctus venom

There is currently no data regarding the toxicity or the in vivo effects of the venom the Aegaeobuthus nigrocinctus species, since it has not been studied thus far according to the best of our knowledge. In the present study, and for the first time, the median lethal dose, the in vivo toxic effects, the histological changes in some of the vital organs were all determined as well as an assessment was made of the histological, biochemical and haematological changes which were caused by the venom injected in mice. The median lethal dose (LD50) of the scorpion venom for mice was found to be 0.38 mg/kg in terms of body weight. The results of the study show that the A. nigrocintus is a potentially lethal scorpion. The evidence related to the venom indicated that it could cause tissue injury in some vital organs. In conclusion, this scorpion venom could cause significant medical complications, and may lead to death, regarding at-risk patients. Therefore, health professionals should be aware of the various scorpion species in their regions and should follow current medical approaches concerning scorpion envenomation.

Protocatechuic acid attenuates chronic unpredictable mild stress induced-behavioral and biochemical alterations in mice

Amelioration of oxidative stress via promoting the endogenous antioxidant system and enhancement of monoamines in brain were the important underlying antidepressant mechanism of protocatechuic acid (PCA). The aim of the present study is to explore the potential antidepressant mechanism(s) PCA in chronic unpredictable mild stress (CUMS) mice. Mice were subjected to CUMS protocol for 4 weeks, and administered with PCA (100 and 200 mg/kg) and fluoxetine (20 mg/kg) for 24 days (from day 8th to 31st). Behavioral (sucrose preference, immobility time, exploratory behavior), and biochemical alterations such as serum corticosterone, brain derived neurotrophic factor (BDNF), inflammatory cytokines, tumor necrosis factor- α (TNF-α), interleukin-6 (IL-6), and antioxidants parameters were investigated. Experimental findings revealed that CUMS subjected mice exhibited significant impairment in behavioral alterations, such as increased immobility time, impaired preference to the sucrose solution, BDNF levels and, serum corticosterone, cytokines, malondialdehyde (MDA) formation with impaired antioxidants in the hippocampus and cerebral cortex. Administration of PCA to CUMS mice attenuated the immobility time, serum corticosterone, cytokines TNF-α, and IL-6, MDA formation and improved sucrose preference, including restoration of BDNF level. Thus, the present findings demonstrated the antidepressant potential of PCA which is largely achieved probably through maintaining BDNF level, and by modulation of the oxidative stress response, cytokines systems, and antioxidant defense system in mice.

Allium cepa fraction attenuates STZ-induced dementia via cholinesterase inhibition and amelioration of oxidative stress in mice.

Background An earlier study demonstrated significant antioxidant and anticholinesterase activities of hydromethanol extract (HME) of Allium cepa. The aim of the study was to investigate the component responsible for these activities followed by an in vivo study. Methods In vitro antioxidant and anticholinesterase activities of standardized ethylacetate fraction (EAF) of HME were assessed. Bioactivity-guided fractionation showed that, as compared with its subfractions, EAF had most significant activity in 2,2-diphenyl-1-picrylhydrazyl and Ellman assays. Thus, EAF was further examined using a streptozotocin (STZ)-induced model of Alzheimer's disease in mice. STZ was injected intracerebroventricularly on days 1 and 3 (3 mg/kg) in mice. EAF was thereafter administered (42, 84, and 168 mg/kg b.w./day p.o.) from days 9 to 22. The Morris water maze test was used to evaluate learning and memory in mice. Acetylcholinesterase (AChE) activity and oxidative stress markers were assessed in the brain homogenates of mice. Additionally, histopathological studies were performed to observe effects in the brain at the cellular level. EAF was standardized based on quercetin and quercetin 4'-O-glucoside content using a validated thin layer chromatography densitometric method. Results STZ produced significant (p < 0.05) memory impairment along with oxidative stress and a cholinergic deficit in mice. EAF treatment ameliorated STZ-induced behavioral deficits and biochemical alterations in mice in a significant and dose-dependent manner. Conclusions Our results show that EAF is efficacious in improving memory and learning via AChE inhibition and antioxidant activity in the mice brain. Thus, AC could be explored further to find out a lead candidate for Alzheimer's disease.

Manganese attenuates the effects of arsenic on neurobehavioral and biochemical changes in mice co-exposed to arsenic and manganese.

An unsafe level of manganese (Mn) was detected in the drinking water in some arsenic (As)-contaminated areas in Bangladesh. Mn is an essential trace element; however, the intake of a higher level of Mn through the drinking water is associated with the development of toxicity in humans. This study was designed to evaluate the effects of As and Mn co-exposure on neurobehavioral and biochemical alterations in a mouse model. Sodium arsenite (10 mg/kg body weight) and manganese chloride tetrahydrate (10 mg/kg body weight) were given to mice individually and in combination with drinking water for 90 days. Results showed that individual As and Mn exposure as well as co-exposure of As and Mn significantly (p < 0.05) reduced the percent of time spent in the open arms when compared with that of control mice. In addition, percent of time spent in open arms significantly (p < 0.05) increased in co-exposed mice compared with As exposure in elevated plus maze (42.05 ± 1.10 versus 38.94 ± 0.66). In the Morris water maze test, the mean time latency to find the platform was longer in metal-treated mice in comparison to that of control mice (p < 0.05). Importantly, the co-exposed group had shorter time when compared with the As-exposed group during the training periods (p < 0.05). Moreover, co-exposed mice stayed significantly (p < 0.05) more time in the target quadrant in the probe trial in comparison with that of As-exposed mice (27.25 ± 1.21 versus 23.83 ± 0.87 s) but less time than control mice (27.25 ± 1.21 versus 43.17 ± 1.49 s). In addition, a significant (p < 0.05) alteration of biochemical parameters such as ALT, AST, ALP, BChE, and SOD as well as urea and creatinine levels were noted in the As-exposed group compared with the control group and Mn significantly (p < 0.05) attenuated the effects of As in co-exposed mice. Therefore, the results of this study suggest that As and Mn may have some antagonistic effect and Mn could attenuate the As-induced neurobehavioral and biochemical alterations in co-exposed mice.

Protein kinase C is involved in the neuroprotective effect of berberine against intrastriatal injection of quinolinic acid-induced biochemical alteration in mice.

Protein kinase C (PKC) shows a neuronal protection effect in neurodegenerative diseases. In this study, we test whether berberine has a positive effect on the activity of PKC in quinolinic acid (QA)‐induced neuronal cell death. We used intrastriatal injections of QA mice model to test the effect of berberine on motor and cognitive deficits, and the PKC signalling pathway. Treatment with 50 mg/kg b.w of berberine for 2 weeks significantly prevented QA‐induced motor and cognitive impairment and related pathologic changes in the brain. QA inhibited the phosphorylation of PKC and its downstream molecules, GSK‐3β, ERK and CREB, enhanced the glutamate level and release of neuroinflammatory cytokines; these effects were attenuated by berberine. We used in vivo infusion of Go6983, a PKC inhibitor to disturb PKC activity in mice brain, and found that the effect of berberine to reverse motor and cognitive deficits was significantly reduced. Moreover, inhibition of PKC also blocked the anti‐excitotoxicity effect of berberine, which is induced by glutamate in PC12 cells and BV2 cells, as well as anti‐neuroinflammatory effect in LPS‐stimulated BV2 cells. Above all, berberine showed neuroprotective effect against QA‐induced acute neurotoxicity by activating PKC and its downstream molecules.

Tolfenamic Acid Attenuates 3-Nitropropionic Acid-Induced Biochemical Alteration in Mice

Tolfenamic acid (TA), a nonsteroidal anti-inflammatory drug, shows neuroprotective effects and alleviates cognitive deficits in transgenic mouse models of Alzheimer's disease. However, whether TA can prevent the biochemical alterations induced by intraperitoneal injection of 3-nitropropionic acid (3-NP) in mice is still unknown. In this study, the striatal lesion area was measured by 2,3,5-triphenyltetrazolium chloride staining. Glutamate, SDH and ATP levels were tested using colorimetric assay kits. The neuroinflammatory cytokine levels were tested by ELISA kits. The expression of synaptic proteins and the subtypes of the NMDA receptor were tested by western blotting. TA was orally administered 10days before 3-NP injection (pretreatment) or on the same day as 3-NP injection (co-treatment). TA pretreatment showed the strongest neuroprotective effects: pretreatment significantly attenuated the 3-NP-induced muscular weakness in the forelimb and alterations in glutamate level, mitochondrial function, and pro-inflammatory cytokine release in the brains of mice. These results suggest that TA has preventive and protective effects on 3-NP-induced neurotoxicity.

Inhibitory effect of bee venom against potassium bromate causing genetic toxicity and biochemical alterations in mice

Background/aim Bee venom (BV) therapy is a highly effective treatment, capable of improving one’s health. The present study attempts to assess the effect of BV on the toxicity of oral administration of potassium bromate (KBrO3) which has been widely used in food and cosmetic industries. Materials and methods Sixty adult male mice were gavaged with KBrO3 at two doses (100 and 200 mg/kg body weight) for 10 days. Afterwards, BV at a dose of 120 μg/kg body weight was injected subcutaneously three times per week for two successive weeks. The genetic study was performed using chromosomal aberration and micronucleus formation in the bone marrow, DNA fragmentation in liver cells and by sperm analysis. In addition, serum biochemical markers such as catalase and malondialdehyde, kidney, and liver functions were assessed. Results The results have shown that KBrO3 caused DNA damage that represented the increase in the frequencies of chromosome abnormalities, micronuclei formation, percentage of DNA fragmentation, and sperm morphological abnormalities. Meanwhile, the results showed that KBrO3 exhibited severe toxicity for antioxidant activities for liver and kidney functions. Conversely, BV significantly decreased the frequencies of DNA damage in all aforementioned parameters induced by KBrO3. In addition, it improved the antioxidant activities and the function of the liver and kidneys. Conclusion BV has a potent ameliorating effect against the KBrO3 hazard impacts in animal tissues especially at higher doses. This observation indicated that BV could be a potential therapeutic agent in the treatment of KBrO3 risk.

Protective Effects of Morin Hydrate on Acute Stress-Induced Behavioral and Biochemical Alterations in Mice.

Introduction:As stress affects the brain both physiologically and chemically, researchers try to find novel anti-stress compounds with beneficial therapeutic effects. In this regard, the effect of stress and its modulation by Morin hydrate was studied using different acute models in mice.Methods:The models employed were anoxic tolerance, swimming endurance, and acute restraint test. Morin hydrate or the vehicle was administered 30 minutes prior to each stress exposure while in the acute restraint test; the animals were pretreated for 7 days with Morin hydrate, vehicle, imipramine, or diazepam before stress exposure. The measured parameters were the onset of convulsion and immobility time in the anoxic tolerance and swimming endurance test, respectively, while in the acute restraint test, the animals were assessed for stress-induced anxiety using the elevated plus maze and depression using the forced swim test. Thereafter blood was withdrawn from the retro-orbital plexus and plasma separated, the brain was also isolated, homogenized, centrifuged, and the supernatant was obtained for biochemical estimation.Results:Morin hydrate (5, 10, 20 mg/kg) produced a significant reduction in immobility time in the swimming endurance test, while significantly increased the anoxic stress tolerance time. Acute restraint stress caused a significant decrease in reduced glutathione levels (which was reversed by Morin hydrate) and increased the level of malondialdehyde, a thiobarbituric acid reactive substance which is an index of oxidative stress and nitrite. These effects were attenuated by Morin hydrate. Also, pretreatment with Morin hydrate attenuates acute restraint stress-associated anxiety and depression, reversed the hyperglycemia evoked by the stressful exposure and normalized serum cholesterol levels.Conclusion:These findings suggest that Morin hydrate exhibits anti-stress effects and may be useful in the relief of stress.

Protective effect of the orientin on noise-induced cognitive impairments in mice

There is increasing evidence that chronic noise stress impairs cognition and induces oxidative stress in the brain. Recently, orientin, a phenolic compound abundant in some fruits, millet, and herbs, has been shown to have antioxidant properties. This study investigated the potential effects of orientin against chronic noise-induced cognitive decline and its underlying mechanisms. A moderate-intensity noise exposure model was used to investigate the effects of orientin on behavior and biochemical alterations in mice. After 3 weeks of the noise exposure, the mice were treated with orientin (20mg/kg and 40mg/kg, oral gavage) for 3 weeks. The chronic noise exposure impaired the learning and memory in mice in the Morris water maze and step-through tests. The noise exposure also decreased exploration and interest in a novel environment in the open field test. The administration of orientin significantly reversed noise-induced alterations in these behavior tests. Moreover, the orientin treatment significantly improved the noise-induced alteration of serum corticosterone and catecholamine levels and oxidative stress in the hippocampus and prefrontal cortex. Furthermore, the orientin treatment ameliorated the noise-induced decrease in brain-derived neurotrophic factor and synapse-associated proteins (synaptophysin and postsynaptic density protein 95) in the hippocampus and prefrontal cortex. Thus, orientin exerts protective effects on noise-induced cognitive decline in mice, specifically by improving central oxidative stress, neurotransmission, and increases synapse-associated proteins. Therefore, supplementation with orientin-enriched food or fruit could be beneficial as a preventive strategy for chronic noise-induced cognitive decline.

Orientin improves depression-like behavior and BDNF in chronic stressed mice.

Oxidative stress is involved in chronic stress-induced depression and the disruption of neurotransmission and neuroplasticity. Recently, orientin, a phenolic compound abundant in some fruits, millet, and herbs, has been shown to have antioxidant properties. This study investigated the potential antidepressant effects of orientin against chronic stress and its underlying mechanisms. The chronic unpredictable mild stress (CUMS) model was used to investigate the effects of orientin on behavior and biochemical alterations in mice. After 2 weeks of the CUMS protocol, the mice were treated with orientin (20 mg/kg and 40 mg/kg, oral gavage) for 3 weeks. Administration of orientin significantly alleviated the CUMS-induced depression-like behavior, including sucrose preference reduction, locomotor activity decline, and hypomotility. Orientin treatment attenuated the oxidative stress markers and increased the concentrations of serotonin and norepinephrine in the hippocampus and prefrontal cortex of CUMS mice. Orientin treatment also increased the brain-derived neurotrophic factor and synapse-associated proteins (synaptophysin and postsynaptic density protein 95) of CUMS mice. Orientin exerts antidepressant-like effects on CUMS mice, specifically by improving central oxidative stress, neurotransmission, and neuroplasticity. Therefore, supplementation with orientin-enriched food or fruit could be beneficial as a preventive strategy for chronic stress-induced depression.

Neuropharmacological effect of novel 5-HT3 receptor antagonist, N-n-propyl-3-ethoxyquinoxaline-2-carboxamide (6n) on chronic unpredictable mild stress-induced molecular and cellular response: Behavioural and biochemical evidences

BackgroundChronic unpredictable stressors can produce a situation similar to human depression and such animal models can be used for the preclinical evaluation of antidepressants. The 5-HT3 receptor antagonists modulate serotonergic pathways and show antidepressant-like effect in various animal models of depression. MethodsIn this study, a novel and potential 5-HT3 receptor antagonist N-n-propyl-3-ethoxyquinoxaline-2-carboxamide (6n) with good Log P (2.52) value and pA2 (7.6) values, synthesized in our laboratory was explore to study the effects on CUMS-induced behavioural and biochemical alterations in mice. Mice were subjected to different stress paradigms daily for a period of 28 days to induce depressive-like behaviour. ResultsCUMS caused depression-like behaviour in mice, as indicated by the significant decrease in sucrose consumption and increase in immobility time in the forced swim test (FST) while there was no significant effect on spontaneous locomotor activity (SLA) observed. In addition it was found that lipid peroxide and nitrite levels were significantly increased, whereas glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) levels were decreased in brain tissue of CUMS-treated mice. Compound 6n (1 and 2mg/kg, po, 21 days) and fluoxetine treatment (20mg/kg, po, 21 days) significantly altered the CUMS-induced behavioural (increased immobility period, reduced sucrose preference) and biochemical (increased lipid peroxidation, increased brain nitrite; decreased GSH, SOD and CAT levels) parameters while there was no significant effect of observed on SLA. ConclusionCompound 6n produced antidepressant-like effects in behavioural despair paradigm in chronically stressed mice by restoring antioxidant enzyme activity up to significant level.

Effect of trimethylgallic acid esters against chronic stress-induced anxiety-like behavior and oxidative stress in mice

BackgroundMany studies have shown that the levels of oxidative stress (increased lipid peroxidation, decreased glutathione levels and endogenous antioxidant enzyme activities) and proinflammatory cytokines (e.g., TNF-α) are increased in patients with chronic fatigue syndrome. Gallic acid and other phenolic compounds are potent antioxidants and inhibitor of cytokine production. The present study was designed to investigate the effect of newly synthesized conjugated esters of trimethylgallic acid in an experimental model of chronic stress. MethodsThe animals were forced to swim individually for a period of 6min every day for 15 days to induce chronic stress. The locomotor activity, anxiety-like behavior, and memory retention were evaluated in chronically stressed animals, followed by biochemical estimations and neuroinflammatory surge in the brain. ResultsChronic treatment with trimethylgallic acid esters for 15 days significantly reversed the chronic stress-induced behavioral (impaired locomotor activity, anxiety-like behavior, and decreased percentage of memory retention), biochemical (increased lipid peroxidation and nitrite levels; decreased glutathione levels, superoxide dismutase and catalase activities), and inflammation surge (serum TNF-α) in stressed mice. ConclusionsThe study revealed that trimethylgallic acid esters could ameliorate chronic stress-induced various behavioral and biochemical alterations in mice, showing protective effects against chronic stress.

Neuropharmacological evaluation of a novel 5-HT3 receptor antagonist (6g) on chronic unpredictable mild stress-induced changes in behavioural and brain oxidative stress parameters in mice.

Aim:The aim of the study was to evaluate a novel 5 HT3 receptor antagonist (6g) on chronic stress induced changes in behavioural and brain oxidative stress parameter in mice. A complicated relationship exists among stressful stimuli, body's reaction to stress and the onset of clinical depression. Chronic unpredictable stressors can produce a situation similar to human depression, and such animal models can be used for the preclinical evaluation of antidepressants.Materials and Methods:In the present study, a novel and potential 5-HT3 receptor antagonist (4-benzylpiperazin-1-yl)(3-methoxyquinoxalin-2-yl) methanone (6g) with good Log P (3.08) value and pA2(7.5) values, synthesized in our laboratory was investigated to study the effects on chronic unpredictable mild stress (CUMS)-induced behavioural and biochemical alterations in mice. Mice were subjected to different stress paradigms daily for a period of 28 days to induce depressive-like behaviour.Results:The results showed that CUMS caused depression-like behaviour in mice, as indicated by the significant (P < 0.05) decrease in sucrose consumption and locomotor activity and increase in immobility the forced swim test. In addition, it was found that lipid peroxidation and nitrite levels were significantly (P < 0.05) increased, whereas glutathione levels, superoxide dismutase and catalase activities decreased in brain tissue of CUMS-treated mice. ‘6g’ (1 and 2 mg/kg, p.o., 21 days) and fluoxetine treatment (20 mg/kg, p.o., 21 days) significantly (P < 0.05) reversed the CUMS-induced behavioural (increased immobility period, reduced sucrose preference and decreased locomotor activity) and biochemical (increased lipid peroxidation; decreased glutathione levels, superoxide dismutase and catalase activities). However fluoxetine treatment (20 mg/kg, p.o., 21 days) significantly decreased the nitrite level in the brain while ‘6g’ (1 and 2 mg/kg, p.o., 21 days) did not show significant (P < 0.05) effect on the nitrite levels in brain.Conclusion:Compound ‘6g’ exerted antidepressant-like effects in behavioural despair paradigm in chronically stressed mice by restoring antioxidant mechanisms.