α-Tocotrienol provides the most potent neuroprotection among vitamin E analogs on cultured striatal neurons

Osakada, Fumitaka; Hashino, Asami; Kume, Toshiaki; Katsuki, Hiroshi; Kaneko, Shuji; Akaike, Akinori

doi:10.1016/j.neuropharm.2004.06.029

Cited by 126 publications

(83 citation statements)

References 35 publications

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“…Taken together, these results demonstrate that tocotrienol mediates its apoptotic effect through the activation of different intracellular signaling mechanisms in different types of cancer cells. Many other investigators have also reported that tocotrienol exhibits anticancer properties by inducing apoptosis (Shah et al 2003;Shah and Sylvester 2004;Takahashi and Loo 2004;Agarwal et al 2004;McIntyre et al 2000aMcIntyre et al , 2000bOsakada et al 2004;Sakai et al 2004;Shun et al 2004). …”

Section: Apoptosis and Tocotrienolmentioning

confidence: 96%

Tocotrienols fight cancer by targeting multiple cell signaling pathways

et al. 2011

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Cancer cells are distinguished by several distinct characteristics, such as self-sufficiency in growth signal, resistance to growth inhibition, limitless replicative potential, evasion of apoptosis, sustained angiogenesis, and tissue invasion and metastasis. Tumor cells acquire these properties due to the dysregulation of multiple genes and associated cell signaling pathways, most of which are linked to inflammation. For that reason, rationally designed drugs that target a single gene product are unlikely to be of use in preventing or treating cancer. Moreover, targeted drugs can cause serious and even life-threatening side effects. Therefore, there is an urgent need for safe and effective promiscuous (multitargeted) drugs. ''Mother Nature'' produces numerous such compounds that regulate multiple cell signaling pathways, are cost effective, exhibit low toxicity, and are readily available. One among these is tocotrienol, a member of the vitamin E family, which has exhibited anticancer properties. This review summarizes data from in vitro and in vivo studies of the effects of tocotrienol on nuclear factor-jB, signal transducer and activator of transcription (STAT) 3, death receptors, apoptosis, nuclear factor (erythroid-derived 2)-like 2 (Nrf2), hypoxia-inducible factor (HIF) 1, growth factor receptor kinases, and angiogenic pathways.

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Section: Apoptosis and Tocotrienolmentioning

confidence: 96%

Tocotrienols fight cancer by targeting multiple cell signaling pathways

et al. 2011

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“…Sen et al (2000) reported that tocotrienols are effective for preventing glutamate-induced neuronal cell death by regulating unique signal transduction. Dsakada et al (2004) demonstrated that tocotrienols purified from palm oil significantly attenuate hydrogen peroxide (H2D2)-induced neurotoxicity. And finally, Choi et al (2010) demonstrated the potential protection of the tocotrienols on neuronal cells, using TRF from grape seed as antioxidant defense systems in tert-butyl hydroperoxide (TBHP)-induced oxidative injury in HepG2 cells.…”

Section: Gso and Oxidative Parametersmentioning

confidence: 99%

Grape seed oil: a potential functional food?

et al. 2015

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“…Primary cultures were prepared from the anterior striatum of fetal Wistar rats (Nihon SLC, Shizuoka) at the 17th -19th days of gestation, according to previously described procedures (16). Briefly, the anterior striatum of fetal rats was removed bilaterally, mechanically dissociated using scalpel blades, and then filtered through a stainless steel mesh.…”

Section: Cell Culturementioning

confidence: 99%

Glutathione Biosynthesis via Activation of the Nuclear Factor E2–Related Factor 2 (Nrf2) – Antioxidant-Response Element (ARE) Pathway Is Essential for Neuroprotective Effects of Sulforaphane and 6-(Methylsulfinyl) Hexyl Isothiocyanate

et al. 2011

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Abstract.Oxidative stress plays pivotal roles in aging, neurodegenerative disease, and pathological conditions such as ischemia. We investigated the effect of sulforaphane and 6-(methysulfinyl) hexyl isothiocyanate (6-HITC), a naturally occurring isothiocyanate, on oxidative stressinduced cytotoxicity using primary neuronal cultures of rat striatum. Pretreatment with sulforaphane and 6-HITC significantly protected against H 2 O 2 -and paraquat-induced cytotoxicity in a concentration-dependent manner. Sulforaphane and 6-HITC induced the translocation of nuclear factor E2-related factor 2 (Nrf2) into the nucleus and increased the expression of γ-glutamylcysteine synthetase (γ-GCS), a rate-limiting enzyme in glutathione synthesis, and the intracellular glutathione content. Treatment with reduced glutathione (GSH) and N-acetyl-L-cysteine, a substance for glutathione synthesis, significantly prevented the cytotoxicity induced by H 2 O 2 and paraquat. Moreover, exposure to L-buthionine-sulfoximine, an irreversible inhibitor of γ-GCS, suppressed the protective effects of sulforaphane and 6-HITC. In contrast, sulforaphane and 6-HITC increased heme oxygenase-1 (HO-1) expression in neurons. However, zinc-protophorphyrin IX, a competitive inhibitor of HO-1, did not influence the protective effects of sulforaphane and 6-HITC. These results suggest that sulforaphane and 6-HITC prevent oxidative stress-induced cytotoxicity in rat striatal cultures by raising the intracellular glutathione content via an increase in γ-GCS expression induced by the activation of the Nrf2-antioxidant response element pathway.

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α-Tocotrienol provides the most potent neuroprotection among vitamin E analogs on cultured striatal neurons

Cited by 126 publications

References 35 publications

Tocotrienols fight cancer by targeting multiple cell signaling pathways

Tocotrienols fight cancer by targeting multiple cell signaling pathways

Grape seed oil: a potential functional food?

Glutathione Biosynthesis via Activation of the Nuclear Factor E2–Related Factor 2 (Nrf2) – Antioxidant-Response Element (ARE) Pathway Is Essential for Neuroprotective Effects of Sulforaphane and 6-(Methylsulfinyl) Hexyl Isothiocyanate

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