2014
DOI: 10.1016/j.brainres.2014.09.033
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Neuroprotection by 6-(methylsulfinyl)hexyl isothiocyanate in a 6-hydroxydopamine mouse model of Parkinson׳s disease

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Cited by 30 publications
(32 citation statements)
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“…Morroni et al studied the neuroprotective effects of 6-(methylsulfinyl)hexyl ITC in a Parkinson s disease mouse model and found that the decrease of apoptotic cell death and the activation of glutathione-dependent antioxidant systems could be underlying a mechanism of beneficial ITC effect [26]. Further investigation of the neuroprotective effect on IMR-32 human neuroblastoma cells was conducted by Trio et al, who concluded that 6-(methylsulfinyl)hexyl ITC can exert a neuroprotective effect by activating the Nrf2-mediated oxidative stress response pathway [27].…”
Section: Cytotoxic Activitymentioning
confidence: 99%
“…Morroni et al studied the neuroprotective effects of 6-(methylsulfinyl)hexyl ITC in a Parkinson s disease mouse model and found that the decrease of apoptotic cell death and the activation of glutathione-dependent antioxidant systems could be underlying a mechanism of beneficial ITC effect [26]. Further investigation of the neuroprotective effect on IMR-32 human neuroblastoma cells was conducted by Trio et al, who concluded that 6-(methylsulfinyl)hexyl ITC can exert a neuroprotective effect by activating the Nrf2-mediated oxidative stress response pathway [27].…”
Section: Cytotoxic Activitymentioning
confidence: 99%
“…A naturally-occurring compound, 6-(methylsulfinyl) hexyl isothiocyanate (6-MITC), was isolated from Wasabia japonica (wasabi), a pungent spice widely used in Japanese food. Several biological activities of 6-MITC have been reported, such as anti-inflammatory [17,18], neuroprotective [19,20], anti-cancer [21][22][23], and chemopreventive effects [24,25]. Our previous publication indicated that 6-MITC and its derivatives may have an inhibitory effect against pancreatic cancer cell growth (including cancer stem cells phenotype) [26].…”
Section: Introductionmentioning
confidence: 99%
“…Leptin was shown to protect the neuroblastoma cells through a PI3K/Akt-dependent pathway 85 , altered Akt, and its downstream target glycogen synthase kinase-3β (GSK-3β) in depression. Meanwhile, a MEK/ERK1/2-induced increase in CREB activation preserved dopaminergic cell survival in proapoptotic conditions 85 , 86 . In-vivo experimentation showed that up to 2 months after neurotoxin exposure, motor behavior is salvaged in leptin-treated animals compared with controls in degeneration of dopaminergic neurons’ environments in part through preservation of nigrostriatal functionality.…”
Section: Leptin In Central Nervous System Diseasementioning
confidence: 99%