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Yoshio Hatori

Researcher at Chiba University

Publications -  6
Citations -  207

Yoshio Hatori is an academic researcher from Chiba University. The author has contributed to research in topics: Phospholipase & Kinase. The author has an hindex of 6, co-authored 6 publications receiving 191 citations. Previous affiliations of Yoshio Hatori include Chulalongkorn University.

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Involvement of μ-opioid receptors in antinociception and inhibition of gastrointestinal transit induced by 7-hydroxymitragynine, isolated from Thai herbal medicine Mitragyna speciosa

TL;DR: The results suggest that mu-opioid receptor mechanisms mediate the antinociceptive effect and inhibition of gastrointestinal transit of 7-hydroxymitragynine, and that this compound induced more potent antinOCiceptive effects and was less constipating than morphine.
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A new indole alkaloid, 7-hydroxyspeciociliatine, from the fruits of Malaysian Mitragyna speciosa and its opioid agonistic activity

TL;DR: The new indole alkaloid isolated from the fruits of Malaysian Mitragyna speciosa Korth was found to have a weak stimulatory effect on μ-opioid receptors and was investigated in guinea-pig ileum experiments.
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New Procedure to Mask the 2,3-π Bond of the Indole Nucleus and Its Application to the Preparation of Potent Opioid Receptor Agonists with a Corynanthe Skeleton

TL;DR: Treatment of indole alkaloids with hypervalent iodine in the presence of ethylene glycol provides 2,3-ethylene glycol bridged adducts that could be converted into the original indoles under mild reductive conditions.
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Nerve growth factor-induced up-regulation of cytosolic phospholipase A2alpha level in rat PC12 cells.

TL;DR: Findings suggest that NGF-induced cPLA(2)alpha expression is regulated by gene transcription via the ERK1/2, p38 MAPK and PKC pathways in PC12 cells.
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Up-regulation of cytosolic phospholipase A2α expression by N,N-diethyldithiocarbamate in PC12 cells; involvement of reactive oxygen species and nitric oxide

TL;DR: The first to demonstrate the up-regulation of cPLA(2)alpha expression by DDC treatment in neuronal cells is shown, which may have a potential role in mediating neurotoxic actions of disulfiram.