Mangiferin ameliorates 6-hydroxydopamineinduced cytotoxicity and oxidative stress in ketamine model of schizophrenia

Rao, V. S. N.; Carvalho, Ana Carla da Silva; Trevisan, Maria Teresa; Andrade, Geanne Matos de; Júnior, Hélio Vn; Moraes, Manoel O. de; Iury, Hemerson I. Magalhães H.; Morais, Talita Cavalcante; Santos, Flávia Almeida

doi:10.1016/s1734-1140(12)70879-4

Cited by 54 publications

(32 citation statements)

References 44 publications

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“…These differences can be evoked by different severity of clinical symptoms or duration of the schizophrenia. The study using magnetic resonance spectrometry showed either a fall of GSH in the cerebrospinal fluid and medial Ketamine-induced schizophrenia to mice " lipid peroxidation (brain) - [125] Ketamine-induced schizophrenia to mice " superoxide (prefrontal cortex) - [127] Ketamine-induced schizophrenia to rats " lipid peroxidation (cerebellum, prefrontal cortex, hippocampus, striatum, cortex) " protein peroxidation (striatum, hippocampus)…”

Section: Clinical Studiesmentioning

confidence: 99%

“…In animal models of schizophrenia, perinatal phencyclidine (an NMDA receptor antagonist) administration increased the level of lipid peroxides in rats [124], while ketamine (an NMDA antagonist) injections to mice increased lipid [125,126] and protein [126] peroxidation and raised superoxide levels [127]. In genetic models, there were either increased levels of oxidized lipids in G72/G30 transgenic schizophrenic mice [128] or elevated cortical ROS production in g-aminobutyric acid-ergic interneuron-specific NMDAR hypofunction mice (Ppp1r2-Cre/ fGluN1 knockout [KO] mice) [129] (Table 1).…”

Section: Animal Studiesmentioning

confidence: 99%

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Oxidative stress as an etiological factor and a potential treatment target of psychiatric disorders. Part 2. Depression, anxiety, schizophrenia and autism

Smaga

Niedzielska

Gawlik

et al. 2015

Pharmacological Reports

221

123

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The pathophysiology of psychiatric diseases, including depression, anxiety, schizophrenia and autism, is far from being fully elucidated. In recent years, a potential role of the oxidative stress has been highlighted in the pathogenesis of neuropsychiatric disorders. A body of clinical and preclinical evidence indicates that psychiatric diseases are characterized by higher levels of oxidative biomarkers and with lower levels of antioxidant defense biomarkers in the brain and peripheral tissues. In this article, we review current knowledge on the role of the oxidative stress in psychiatric diseases, based on clinical trials and animal studies, in addition, we analyze the effects of drug-induced modulation of oxidative balance and explore pharmacotherapeutic strategies for oxidative stress reduction.

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Section: Clinical Studiesmentioning

confidence: 99%

Section: Animal Studiesmentioning

confidence: 99%

Oxidative stress as an etiological factor and a potential treatment target of psychiatric disorders. Part 2. Depression, anxiety, schizophrenia and autism

Smaga

Niedzielska

Gawlik

et al. 2015

Pharmacological Reports

221

123

View full text Add to dashboard Cite

show abstract

“…Oxidative stress has been reported to modulate several behaviors including learning and memory function (Alzoubi et al, 2012; Alzoubi et al, 2013a; Alzoubi et al, 2013b), anxiety- (Allam et al, 2013; Hovatta et al, 2005; Masood et al, 2009; Salim et al, 2010a; Salim et al, 2011), depression- (Brocardo et al, 2012; Leonard and Maes, 2012; Pedreanez et al, 2011), mania- (Macedo et al, 2013), nociceptive- (Arcan et al, 2012) and schizophrenia- (Rao et al, 2012) like behaviors. We also measured the effect of social defeat-induced stress on oxidative stress within three critical brain areas, considered vital for depression, anxiety and cognition, namely, hippocampus, amygdala and prefrontal cortex (McEwen et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Depression, anxiety-like behavior and memory impairment are associated with increased oxidative stress and inflammation in a rat model of social stress

Patki¹,

Solanki²,

Atrooz³

et al. 2013

Brain Research

328

213

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In the present study, we have examined the behavioral and biochemical effect of induction of psychological stress using a modified version of the resident-intruder model for social stress (social defeat). At the end of the social defeat protocol, body weights, food and water intake were recorded, depression and anxiety-like behaviors as well as learning-memory function was examined. Biochemical analysis including oxidative stress measurement, inflammatory markers and other molecular parameters, critical to behavioral effects were examined. We observed a significant decrease in the body weight in the socially defeated rats as compared to the controls. Furthermore, social defeat increased anxiety-like behavior and caused memory impairment in rats (P<0.05). Socially defeated rats made significantly more errors in long term memory tests (P<0.05) as compared to control rats. Furthermore, brain extracellular signal-regulated kinase-1/2 (ERK1/2), and an inflammatory marker, interleukin (IL)-6 were activated (P<0.05), while the protein levels of glyoxalase (GLO)-1, glutathione reductase (GSR)-1, calcium/calmodulin-dependent protein kinase type (CAMK)-IV, cAMP-response-element-binding protein (CREB) and brain-derived neurotrophic factor (BDNF) were significantly less (P<0.05) in the hippocampus, but not in the prefrontal cortex and amygdala of socially defeated rats, when compared to control rats. We suggest that social defeat stress alters ERK1/2, IL-6, GLO1, GSR1, CAMKIV, CREB, and BDNF levels in specific brain areas, leading to oxidative stress-induced anxiety-depression-like behaviors and as well as memory impairment in rats.

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“…A review from Mirza et al, 2013, also indicated that the antioxidant activity of MF is majorly contributed by catechol moiety (iron complexing capacity), which inhibit the production of free radicals by inhibiting the conversion of Fe 2+ to Fe 3+ complex and that would be the reason for maintaining the redox balance by elevating antioxidant status in MF treated pups. Supplementation of MF for 7 days probably eases oxidative stress and lipid peroxidation as well as protects BBB in schizophrenia mice model (Rao et al, 2012 Existing evidence suggest that impaired antioxidant with elevated free radicals (oxidative stress) and the neuroinflammatory response is considered to be the major reason for HIE (Sadeghnia et al, 2012;Slemmer at al., 2008). Both the events (oxidative stress and inflammation) are interconnected with one another.…”

Section: Groupmentioning

confidence: 99%

Neurotherapeutic effect of mangiferin against hypoxic–ischemic encephalopathy in neonatal rats

Lv¹,

Wang²,

Hu³

et al. 2016

Afr. J. Trad. Compl. Alt. Med.

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Background: Hypoxic-ischemic encephalopathy (HIE) in perinatal condition is highly associated with mortality and several neurological disabilities. The present experiment was blueprinted to ascertain the protective efficacy of mangiferin (MF) against hypoxic-ischemic brain injury in neonatal rats. Materials and Methods: Fourth six neonatal rats (pups) were randomly separated into four groups as a sham group that received only water (control; n=12), pups exposed to Hypoxic-ischemic (HI) insult (HI group-II; n=11), pups receiving 20 (MF 20+HI-III; n=11) or 40 (MF 40+HI-IV; n=12) mg/kg b. wt of MF dissolved in water via i.p. for 7 consecutive days as pretreatment regimen before HI insult as well as one-time post treatment after HI insult. Results: MF pretreatment for seven days considerably attenuated the cerebral infarct size, edema level, lipid peroxidation (MDA), inflammatory markers (TNF-α, IL-1β, IL-6, and NF-p65 subunit) as well as greatly ameliorated the antioxidant activities of catalase (CAT), superoxide dismutase (SOD), and glutathione reductase (GSH) and thereby maintaining the redox balance. The number of viable neuronal count (nissl bodies) was exponentially increased on administration with both the dosages of MF. Both the dosages showed substantial protection against HIE, however, 40 mg of MF exhibit superior neuroprotection in equivalence with 20 mg of MF. Conclusion:The results of the present study distinctly proving the beneficial effect of MF against HIE by concomitantly improving neuronal count and antioxidant status. Hence, we recommend MF might be used for treating neonatal HIE with some standard drugs.

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Mangiferin ameliorates 6-hydroxydopamineinduced cytotoxicity and oxidative stress in ketamine model of schizophrenia

Abstract: Mangiferin has a neurocytoprotective role related, at least in part, to an antioxidant and anti-inflammatory mechanism, which could be explored for more effective therapies of schizophrenia and other neurodegenerative diseases.

Cited by 54 publications

References 44 publications

Oxidative stress as an etiological factor and a potential treatment target of psychiatric disorders. Part 2. Depression, anxiety, schizophrenia and autism

Oxidative stress as an etiological factor and a potential treatment target of psychiatric disorders. Part 2. Depression, anxiety, schizophrenia and autism

Depression, anxiety-like behavior and memory impairment are associated with increased oxidative stress and inflammation in a rat model of social stress

Neurotherapeutic effect of mangiferin against hypoxic–ischemic encephalopathy in neonatal rats

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