Curcumin protects axons from degeneration in the setting of local neuroinflammation

Tegenge, Million Adane; Rajbhandari, Labchan; Shrestha, Shiva; Mithal, Aditya; Hosmane, Suneil; Venkatesan, Arun

doi:10.1016/j.expneurol.2013.12.016

Cited by 72 publications

(40 citation statements)

References 48 publications

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“…2c). On the other hand, higher concentration of curcumin was cytotoxic (14). At a dose ≥10 µM, a substantially suppressive eff ect occurred (Fig.…”

Section: Eff Ect Of Glutamate Curcumin and Combined Therapy On The Cmentioning

confidence: 99%

“…In conjunction with stem cell therapy, curcumin synergistically improved recovery from acute traumatic spinal cord injury (SCI) (13), underlying the potential regenerative action of curcumin if appropriately mediated by the neural stem cells. Benefi cial protection of axons from degeneration by suppressing the local neuroinfl ammation is also a ribu ed to curcumin (14). Curcumin rescued α-synuclein-induced cell death (15).…”

Section: Introductionmentioning

confidence: 99%

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Curcumin-Protected PC12 Cells Against Glutamate-Induced Oxidative Toxicity

Chang

Chen

Yü

et al. 2014

Food. Technol. Biotechnol.

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SummaryGlutamate is a major excitatory neurotransmi er present in the central nervous system. The glutamate/cystine antiporter system x c -connects the antioxidant defense with neurotransmission and behaviour. Overactivation of ionotropic glutamate receptors induces neuronal death, a pathway called excitotoxicity. Glutamate-induced oxidative stress is a major contributor to neurodegenerative diseases including cerebral ischemia, Alzheimer's and Huntington's disease. Curcuma has a wide spectrum of biological activities regarding neuroprotection and neurocognition. By reducing the oxidative damage, curcumin a enuates a spinal cord ischemia-reperfusion injury, seizures and hippocampal neuronal loss. The rat pheochromocytoma (PC12) cell line exhibits many characteristics useful for the study of the neuroprotection and neurocognition. This investigation was carried out to determine whether the neuroprotective eff ects of curcumin can be observed via the glutamate-PC12 cell model. Results indicate that glutamate (20 mM) upregulated glutathione peroxidase 1, glutathione disulphide, Ca 2+ infl ux, nitric oxide production, cytochrome c release, Bax/Bcl-2 ratio, caspase-3 activity, lactate dehydrogenase release, reactive oxygen species, H 2 O 2 , and malondialdehyde; and downregulated glutathione, glutathione reductase, superoxide dismutase and catalase, resulting in enhanced cell apoptosis. Curcumin alleviates all these adverse eff ects. Conclusively, curcumin can eff ectively protect PC12 cells against the glutamate-induced oxidative toxicity. Its mode of action involves two pathways: the glutathione-dependent nitric oxide-reactive oxygen species pathway and the mitochondria-dependent nitric oxide-reactive oxygen species pathway.

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“…2c). On the other hand, higher concentration of curcumin was cytotoxic (14). At a dose ≥10 µM, a substantially suppressive eff ect occurred (Fig.…”

Section: Eff Ect Of Glutamate Curcumin and Combined Therapy On The Cmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Curcumin-Protected PC12 Cells Against Glutamate-Induced Oxidative Toxicity

Chang

Chen

Yü

et al. 2014

Food. Technol. Biotechnol.

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“…A four-well polydimethylsiloxanebased microfluidic device comprised of two compartments (length = 8 mm, width = 1 mm) separated by an array of 200 microchannels (length = 500 μm, width = 10 μm, height = 2.5 μm) (Fig. 1) was fabricated as previously described (23). We previously showed that these devices allow selective growth of axons in one compartment, enable isolation of cell soma from their axons, and allow independent manipulation of somal and axonal compartments (24)(25)(26).…”

Section: Significancementioning

confidence: 99%

In vitro system using human neurons demonstrates that varicella-zoster vaccine virus is impaired for reactivation, but not latency

Sadaoka

Depledge

Rajbhandari

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

104

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Varicella-zoster virus (VZV) establishes latency in human sensory and cranial nerve ganglia during primary infection (varicella), and the virus can reactivate and cause zoster after primary infection. The mechanism of how the virus establishes and maintains latency and how it reactivates is poorly understood, largely due to the lack of robust models. We found that axonal infection of neurons derived from hESCs in a microfluidic device with cell-free parental Oka (POka) VZV resulted in latent infection with inability to detect several viral mRNAs by reverse transcriptase-quantitative PCR, no production of infectious virus, and maintenance of the viral DNA genome in endless configuration, consistent with an episome configuration. With deep sequencing, however, multiple viral mRNAs were detected. Treatment of the latently infected neurons with Ab to NGF resulted in production of infectious virus in about 25% of the latently infected cultures. Axonal infection of neurons with vaccine Oka (VOka) VZV resulted in a latent infection similar to infection with POka; however, in contrast to POka, VOka-infected neurons were markedly impaired for reactivation after treatment with Ab to NGF. In addition, viral transcription was markedly reduced in neurons latently infected with VOka compared with POka. Our in vitro system recapitulates both VZV latency and reactivation in vivo and may be used to study viral vaccines for their ability to establish latency and reactivate. varicella-zoster virus | varicella vaccine | reactivation | latency | herpesvirus V aricella-zoster virus (VZV) is a member of Alphaherpesvirinae, characterized by neurotropism and lifelong latent infection in human dorsal root, cranial nerve, and enteric ganglia (1). During primary infection (varicella), VZV gains access to sensory neurons by two potential routes: retrograde axonal transport from cutaneous lesions or infection of neurons by virus-infected T cells circulating through the body (2). The virus then establishes latency in neurons, and months to years later, when VZV-specific T cells decline, the virus can reactivate to cause herpes zoster.VZV is the only human herpesvirus for which a licensed vaccine is approved, and the live-attenuated vaccine Oka (VOka) virus is effective in preventing both varicella and zoster. VOka was derived from WT parental Oka (POka) by propagation in human embryonic lung cells, guinea pig embryo fibroblasts, and human fibroblasts (3, 4). VOka is a genetic mixture of at least eight genotypes (5), and, initially, the genomes of POka and VOka were found to differ by 42 nucleotides and 20 amino acids (6). A recent study using deep sequencing identified 165 additional nucleotide changes in VOka, although most changes were presence in <10% of viral genomes (7). Attenuation of VOka is postulated to be due to mutations in multiple regions of the genome (8, 9).Despite numerous studies, the mechanisms for establishment and maintenance of VZV latency and subsequent reactivation remain poorly understood, primarily due to the lack of ...

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“…Indeed, anti-inflammatory effects of curcumin vis-à-vis suppression of IL-1β, tumor necrosis factor TNF-α, (Gupta et al 2014; Yuan et al 2015), and the nuclear factor NF-κB, considered a prototypical pro-inflammatory signaling pathway (Yang et al Yang et al 2014b; Yuan et al 2015), as well as intracellular components of glial fibrillary acidic protein (GFAP), considered a marker of gliosis (Yuan et al 2015), have been reported. Thus, curcumin may exert a neuroprotective effect against the 6-OHDA-induced rat model of PD (Yang et al 2014aa) and may also protect axons from degeneration in the setting of local neuroinflammation (Tegenge et al 2014). In addition, curcumin may ameliorate the adverse effects of the neurotoxin N -methyl N -nitrosourea in the cerebrum and cerebellum of mice (Singla and Dhawan 2012) and may exert a neuroprotective effect against ischemic spinal cord injury by decreasing inducible nitric oxide synthase as well as N -methyl- d -aspartate receptor expression (Zhang et al 2013).…”

Section: Curcuminmentioning

confidence: 99%

Duality of Antidepressants and Neuroprotectants

Tizabi

2015

Neurotox Res

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The co-morbidity of neuropsychiatric disorders, particularly major depressive disorder (MDD) with neurodegenerative diseases, in particular Parkinson’s disease (PD) is now well recognized. Indeed, it is suggested that depressive disorders, especially in late life, may be an indication of latent neurodegeneration. Thus, it is not unreasonable to expect that deterrents of MDD may also deter the onset and/or progression of the neurodegenerative diseases including PD. In this review, examples of neuroprotective efficacy of established as well as prospective antidepressants are provided. Conversely, mood-regulating effects of some neuroprotective drugs are also presented. Thus, in addition to currently used antidepressants, ketamine, nicotine, curcumin, and resveratrol are discussed for their dual efficacy. In addition, potential neurobiological substrates for their actions are presented. It is concluded that pharmacological developments of mood-regulating or neuroprotective drugs can have cross benefit in co-morbid conditions of neuropsychiatric and neurodegenerative disorders and that inflammatory and neurotrophic factors play important roles in both conditions.

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Curcumin protects axons from degeneration in the setting of local neuroinflammation

Cited by 72 publications

References 48 publications

Curcumin-Protected PC12 Cells Against Glutamate-Induced Oxidative Toxicity

Curcumin-Protected PC12 Cells Against Glutamate-Induced Oxidative Toxicity

In vitro system using human neurons demonstrates that varicella-zoster vaccine virus is impaired for reactivation, but not latency

Duality of Antidepressants and Neuroprotectants

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