Valproate inhibits oxidative damage to lipid and protein in primary cultured rat cerebrocortical cells

Wang, J.F; Azzam, J.E; Young, L. Trevor

doi:10.1016/s0306-4522(02)00655-3

Cited by 98 publications

(61 citation statements)

References 44 publications

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“…These beneficial effects were blocked, moreover, by curcumin (Hiroi et al, 2005), an AP-1 inhibitor. On the other hand, VPA pretreatment also upregulated this ER stress protein (Wang et al, 1999Bown et al, 2000;Hiroi et al, 2005), and induced similar protective effects against ER stress in PC12 cells (Hiroi et al, 2005), as well as oxidative damage in primary cultured rat cerebrocortical cells (Wang et al, 2003). Because ER dysfunction has been linked to impaired synaptic plasticity and to the pathophysiology of diseases, such as BD (Hough et al, 1999;Hayashi et al, 2009), AD (Mattson et al, 2000), and cerebral ischemia (Mattson et al, 2000), the induction of GRP78 by lithium and VPA against ER stress may well be clinically relevant.…”

Section: E Protein Quality Control Mechanismsmentioning

confidence: 93%

Therapeutic Potential of Mood Stabilizers Lithium and Valproic Acid: Beyond Bipolar Disorder

et al. 2013

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Section: E Protein Quality Control Mechanismsmentioning

confidence: 93%

Therapeutic Potential of Mood Stabilizers Lithium and Valproic Acid: Beyond Bipolar Disorder

et al. 2013

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“…Others have supported the antioxidant effects of lithium, but have not found it able to prevent stress-induced oxidative damage in rats (de Vasconcellos et al, 2006). Treatment with valproate has been shown to inhibit lipid peroxidation and protein oxidation in primary cultured rat cerebrocortical cells exposed to an oxidant (Wang et al, 2003). Using similar cell cultures, treatment with lithium or valproate was also shown to inhibit the glutamate-induced intracellular calcium release, lipid peroxidation, protein oxidation, DNA fragmentation and cell death (Shao et al, 2005).…”

Section: Preclinical Studiesmentioning

confidence: 99%

Oxidative stress in psychiatric disorders: evidence base and therapeutic implications

Berk

Dean

et al. 2008

Int. J. Neuropsychopharm.

881

569

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Oxidative stress has been implicated in the pathogenesis of diverse disease states, and may be a common pathogenic mechanism underlying many major psychiatric disorders, as the brain has comparatively greater vulnerability to oxidative damage. This review aims to examine the current evidence for the role of oxidative stress in psychiatric disorders, and its academic and clinical implications. A literature search was conducted using the Medline, Pubmed, PsycINFO, CINAHL PLUS, BIOSIS Previews, and Cochrane databases, with a time-frame extending to September 2007. The broadest data for oxidative stress mechanisms have been derived from studies conducted in schizophrenia, where evidence is available from different areas of oxidative research, including oxidative marker assays, psychopharmacology studies, and clinical trials of antioxidants. For bipolar disorder and depression, a solid foundation for oxidative stress hypotheses has been provided by biochemical, genetic, pharmacological, preclinical therapeutic studies and one clinical trial. Oxidative pathophysiology in anxiety disorders is strongly supported by animal models, and also by human biochemical data. Pilot studies have suggested efficacy of N-acetylcysteine in cocaine dependence, while early evidence is accumulating for oxidative mechanisms in autism and attention deficit hyperactivity disorder. In conclusion, multi-dimensional data support the role of oxidative stress in diverse psychiatric disorders. These data not only suggest that oxidative mechanisms may form unifying common pathogenic pathways in psychiatric disorders, but also introduce new targets for the development of therapeutic interventions.

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“…Among several multi-member families of Hsps, Hsp70 is one of the best characterized endogenous factors involved in protecting cells from injury under various pathological conditions [10]. Several pharmacological agents, such as valproic acid (VPA), a clinical used drug for the treatment of seizures and bipolar mood disorder [11][12][13], have been demonstrated to increase resistance to injury caused by a variety of insults through the induction of Hsp70 [14].…”

Section: Introductionmentioning

confidence: 99%

Valproic acid‐mediated Hsp70 induction and anti‐apoptotic neuroprotection in SH‐SY5Y cells

Pan

Xie

et al. 2005

FEBS Letters

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Valproic acid (VPA), an anticonvulsant and moodstabilizing drug, has been reported to exert neuroprotection against a variety of insults. We now show that VPA attenuates rotenone (a potent complex I inhibitor)-induced apoptosis through the induction of heat shock protein 70, which may interact with apoptotic-protease-activating factor 1. Activation of p-Akt, p-Bcl-2, as well as p-Erk1/2 by VPA may be co-contributors to the protection.

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Valproate inhibits oxidative damage to lipid and protein in primary cultured rat cerebrocortical cells

Cited by 98 publications

References 44 publications

Therapeutic Potential of Mood Stabilizers Lithium and Valproic Acid: Beyond Bipolar Disorder

Therapeutic Potential of Mood Stabilizers Lithium and Valproic Acid: Beyond Bipolar Disorder

Oxidative stress in psychiatric disorders: evidence base and therapeutic implications

Valproic acid‐mediated Hsp70 induction and anti‐apoptotic neuroprotection in SH‐SY5Y cells

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