Mechanism for the protective effect of resveratrol against oxidative stress-induced neuronal death

Fukui, Masayuki; Choi, Hye Joung; Zhu, Bao Ting

doi:10.1016/j.freeradbiomed.2010.06.002

Cited by 173 publications

(95 citation statements)

References 65 publications

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“…When the same dose of resveratrol was injected via LP, a five-fold higher peak drug concentration (7.700± 0.734 nmol/g; 65.662± 6.259 μM) was observed in the whole brain. According to previous reports, resveratrol at this concentration elicits protective effects to glial cells exposed to lipopolysaccharide [38], to neurons under oxidative stress [26,39] and to neurons after traumatic brain injury [28]. Trans-resveratrol molecules can be biotransformed to less active metabolites when they arrive in target organs [40].…”

Section: Discussionmentioning

confidence: 92%

Diffusion Efficiency and Bioavailability of Resveratrol Administered to Rat Brain by Different Routes: Therapeutic Implications

Shu

Wang

et al. 2015

Neurotherapeutics

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Resveratrol possesses anti-tumor activities against central nervous system (CNS) tumors in vitro but has not yet been used clinically due to its low bioavailability, particularly in the CNS. This study thus aimed to elucidate brain bioavailability of trans-resveratrol by monitoring brain concentrations and dwell times following administration of resveratrol through intragastric, intraperitoneal, external carotid artery/ ECA and intrathecal routes. In parallel, we evaluated the biological responses of rat RG2 glioblastoma cells as well as RG2-formed rat intracranial glioblastomas treated with resveratrol via intrathecal administration. The results revealed that resveratrol was detected in rat brains except when administered systemically. Intrathecal administration of reseveratrol led to abundant apoptotic foci and increased staining of the autophagy proteins, LC-3 and Beclin-1 and shrinkage of the intracranial tumors. In conclusion, the BBB penetrability of resveratrol is remarkably increased by intracthecal administration. Regular short-term resveratrol treatments suppress growth and enhance autophagic and apoptotic activities of rat RG2 glioblastoma cells in vitro and in vivo. Therefore, intrathecal administration of resveratrol could be an optimal intervention approach in the adjuvant management of brain malignancies.

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Section: Discussionmentioning

confidence: 92%

Diffusion Efficiency and Bioavailability of Resveratrol Administered to Rat Brain by Different Routes: Therapeutic Implications

Shu

Wang

et al. 2015

Neurotherapeutics

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“…Patients with PD lack effective therapies that halt neurodegenerative processes and can only be treated for clinical symptoms [23], reinforcing the need to better understand the biological processes that underlie the neurodegeneration [24]. Increasing evidence suggests that salidroside reduces the levels of ROS, which have been linked to the pathogenesis of many diseases [25] including diabetes, cardiovascular disease, and degenerative disease.…”

Section: Discussionmentioning

confidence: 99%

Salidroside Protects Against 6-Hydroxydopamine-Induced Cytotoxicity by Attenuating ER Stress

et al. 2016

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Parkinson's disease (PD) is a neurodegenerative disease characterized by a persistent decline of dopaminergic (DA) neurons in the substantia nigra pars compacta. Despite its frequency, effective therapeutic strategies that halt the neurodegenerative processes are lacking, reinforcing the need to better understand the molecular drivers of this disease. Importantly, increasing evidence suggests that the endoplasmic reticulum (ER) stress-induced unfolded protein response is likely involved in DA neuronal death. Salidroside, a major compound isolated from Rhodiola rosea L., possesses potent antioxidative stress properties and protects against DA neuronal death. However, the underlying mechanisms are not well understood. In the present study, we demonstrate that salidroside prevents 6-hydroxydopamine (6-OHDA)-induced cytotoxicity by attenuating ER stress. Furthermore, treatment of a DA neuronal cell line (SN4741) and primary cortical neurons with salidroside significantly reduced neurotoxin-induced increases in cytoplasmic reactive oxygen species and calcium, both of which cause ER stress, and cleaved caspase-12, which is responsible for ER stress-induced cell death. Together, these results suggest that salidroside protects SN4741 cells and primary cortical neurons from 6-OHDA-induced neurotoxicity by attenuating ER stress. This provides a rationale for the investigation of salidroside as a potential therapeutic agent in animal models of PD.

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“…This effect could be related, at least partially, to the release of a guanine-based purine after astrocytic hypoglycemic insults [6], its trophic properties and ability to stimulate astrocyte proliferation [84], its modulatory effects on the glutamatergic system [3], and its antioxidant properties. Additionally, guanosine promotes the activation of the PI3K signaling pathway, upstream of glycogen synthase kinase 3, which may regulate the glucose uptake, ROS levels and, thus, cell survival [13,85,86].…”

Section: Discussionmentioning

confidence: 99%

Gliopreventive effects of guanosine against glucose deprivation in vitro

Quincozes‐Santos

Bobermin

Souza

et al. 2013

Purinergic Signalling

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Guanosine, a guanine-based purine, is recognized as an extracellular signaling molecule that is released from astrocytes and confers neuroprotective effects in several in vivo and in vitro studies. Astrocytes regulate glucose metabolism, glutamate transport, and defense mechanism against oxidative stress. C6 astroglial cells are widely used as an astrocyte-like cell line to study the astrocytic function and signaling pathways. Our previous studies showed that guanosine modulates the glutamate uptake activity, thus avoiding glutamatergic excitotoxicity and protecting neural cells. The goal of this study was to determine the gliopreventive effects of guanosine against glucose deprivation in vitro in cultured C6 cells. Glucose deprivation induced cytotoxicity, an increase in reactive oxygen and nitrogen species (ROS/RNS) levels and lipid peroxidation as well as affected the metabolism of glutamate, which may impair important astrocytic functions. Guanosine prevented glucose deprivation-induced toxicity in C6 cells by modulating oxidative and nitrosative stress and glial responses, such as the glutamate uptake, the glutamine synthetase activity, and the glutathione levels. Glucose deprivation decreased the level of EAAC1, the main glutamate transporter present in C6 cells. Guanosine also prevented this effect, most likely through PKC, PI3K, p38 MAPK, and ERK signaling pathways. Taken together, these results show that guanosine may represent an important mechanism for protection of glial cells against glucose deprivation. Additionally, this study contributes to a more thorough understanding of the glial-and redox-related protective properties of guanosine in astroglial cells.

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Mechanism for the protective effect of resveratrol against oxidative stress-induced neuronal death

Cited by 173 publications

References 65 publications

Diffusion Efficiency and Bioavailability of Resveratrol Administered to Rat Brain by Different Routes: Therapeutic Implications

Diffusion Efficiency and Bioavailability of Resveratrol Administered to Rat Brain by Different Routes: Therapeutic Implications

Salidroside Protects Against 6-Hydroxydopamine-Induced Cytotoxicity by Attenuating ER Stress

Gliopreventive effects of guanosine against glucose deprivation in vitro

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