Protective effect of desipramine, venlafaxine and trazodone against experimental animal model of transient global ischemia: Possible involvement of NO–cGMP pathway

Gaur, Vaibhav; Kumar, Anil

doi:10.1016/j.brainres.2010.07.004

Cited by 35 publications

(19 citation statements)

References 44 publications

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“…The present study confirmed that Bay 60-7550 regulated the hippocampal and amygdaloid SOD expression, which were accompanied by elevation of p-VASP ser239 , an index of cGMP-PKG signaling. Desipramien and diazepam were also able to reverse the changes of p-VASP ser239 induced by CUS, agreeing with several previous findings stating that neuroprotective effects of desipramine and diazepam involved NO-cGMP signaling [47,48]. …”

Section: Discussionsupporting

confidence: 90%

Protective effects of phosphodiesterase 2 inhibitor on depression- and anxiety-like behaviors: Involvement of antioxidant and anti-apoptotic mechanisms

Ding

Zhang

Masood

et al. 2014

Behavioural Brain Research

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Stress occurs in everyday life, but the relationship between stress and the onset or development of depression/anxiety remains unknown. Increasing evidence suggests that the impairment of antioxidant defense and the neuronal cell death are important in the process of emotional disorders. Chronic stress impairs the homeostasis of antioxidants/oxidation, which results in the aberrant stimulation of the cell cycle proteins where cGMP-PKG signaling is thought to have an inhibitory role. Phosphodiesterase 2 (PDE2) is linked to cGMP-PKG signaling and highly expressed in the limbic brain regions including hippocampus and amygdala, which may play important roles in the treatment of depression and anxiety. To address the possible effects of PDE2 inhibitors on depression-/anxiety-like behaviors and the underlying mechanisms, Bay 60-7550 (0.75, 1.5 and 3 mg/kg, i.p.) was administered 30 min before chronic stress. The results suggested that Bay 60-7550 not only restored the behavioral changes but also regulated Cu/Zn superoxide dismutase (SOD) levels differentially in hippocampus and amygdala, which were increased in the hippocampus while decreased in the amygdala. It was also significant that Bay 60-7550 regulated the abnormalities of pro- and anti-apoptotic components, such as Bax, Caspase 3 and Bcl-2, and the indicator of PKG signaling characterized by pVASPser239, in these two brain regions. The results suggested that Bay 60-7550 is able to alleviate oxidative stress and mediate part of the apoptotic machinery in neuronal cells possibly through SOD-cGMP/PKG-anti-apoptosis signaling and that inhibition of PDE2 may represent a novel therapeutic target for psychiatric disorders, such as depression and anxiety.

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Section: Discussionsupporting

confidence: 90%

Protective effects of phosphodiesterase 2 inhibitor on depression- and anxiety-like behaviors: Involvement of antioxidant and anti-apoptotic mechanisms

Ding

Zhang

Masood

et al. 2014

Behavioural Brain Research

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“…For example, beneficial effects of fluoxetine in reducing oxidative stress in brains (Omar M.E. Abdel-Salam 2011), shielding effects of desipramine against ischemia/reperfusion-induced oxidative stress in mice brain(Gaur & Kumar 2010), the protective role of venlafaxine against stress-induced oxidative neuronal DNA damage (Abdel-Wahab & Salama 2011), and the effect of deprenyl in protecting substantia nigra neurons from oxidative stress (Wu et al 1993) have been reported. Coenzyme Q10 is a fat-soluble vitamin-like substance and possesses antidepressant activity.…”

Section: Effects Of Antidepressants Against Oxidative Dna Damagementioning

confidence: 99%

DNA Damage in Major Psychiatric Diseases

et al. 2016

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Human cells are exposed to exogenous insults and continuous production of different metabolites. These insults and unwanted metabolic products might interfere with the stability of genomic DNA. Recently many studies demonstrated that different psychiatric disorders show substantially high level of oxidative DNA damage in the brain accompanied with morphological and functional alterations. It reveals that damaged genomic DNA may contribute to the pathophysiology of these mental illnesses. Here we review the role of oxidative damage and reduced antioxidant ability in some vastly studied psychiatric disorders and emphasize the inclusion of treatment options involving DNA repair. In addition, while most currently used antidepressants are based on the manipulation of the neurotransmitter regulation in managing different mental abnormalities, they are able to prevent or reverse neurotoxin-induced DNA damage. Therefore, it may be plausible to target on genomic DNA alterations for psychiatric therapies, which is of pivotal importance for future anti-psychiatric drug development.

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“…This cell damage has been shown to be of diffused nature and spread throughout the brain including the hippocampus and the motor cortex (Jenkins et al 1981;Dobkin 1991;Yamamoto et al 2009). Bilateral common carotid artery occlusion (BCCAO) model which is used in the present study is one of the widely used experimental models of partial global cerebral ischaemia (Yanpallewar et al 2005;Gaur et al 2009;Gaur and Kumar 2010c).…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective potentials of candesartan, atorvastatin and their combination against stroke induced motor dysfunction

Gaur

Kumar

2010

Inflammopharmacol

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Cerebral ischaemia is a leading cause of death and disability. The objective of the present investigation was to explore the neuroprotective potentials of candesartan and atorvastatin alone and their combination against the cerebral ischaemia induced behavioral, biochemical, and mitochondrial dysfunction. Male Wistar rats (200-220 g) were subjected to bilateral common carotid artery occlusion for 30 min followed by 24 h reperfusion. Candesartan (0.1 and 0.3 mg/kg) and atorvastatin (10 and 20 mg/kg) were pretreated for 7 days before animals were subjected to ischaemia reperfusion injury. Various behavioral tests (locomotor activity and rotarod performance), biochemical parameters (Malondialdehyde levels, nitrite concentration, superoxide dismutase and catalase activity, redox ratio, and GST) and mitochondrial enzyme (Complex I, II, III, and IV) dysfunctions were measured in cerebral cortex, striatum and hippocampus of the ischaemic brain. Seven days candesartan (0.1 and 0.3 mg/kg) or atorvastatin (10 and 20 mg/kg) pretreatment significantly attenuated neurobehavioral alterations, oxidative damage and restored mitochondrial enzyme dysfunction as compared to control (I/R) group. Further, combined treatment of candesartan (0.1 mg/kg) and atorvastatin (10 mg/kg) significantly potentiated their protective effect which was significant as compared to their effect alone. Present study suggests the protective effect of candesartan and atorvastatin and their combination against ischaemia reperfusion induced behavioral and biochemical alterations in rats.

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Protective effect of desipramine, venlafaxine and trazodone against experimental animal model of transient global ischemia: Possible involvement of NO–cGMP pathway

Cited by 35 publications

References 44 publications

Protective effects of phosphodiesterase 2 inhibitor on depression- and anxiety-like behaviors: Involvement of antioxidant and anti-apoptotic mechanisms

Protective effects of phosphodiesterase 2 inhibitor on depression- and anxiety-like behaviors: Involvement of antioxidant and anti-apoptotic mechanisms

DNA Damage in Major Psychiatric Diseases

Neuroprotective potentials of candesartan, atorvastatin and their combination against stroke induced motor dysfunction

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