Neuroprotective effect of fraxetin and myricetin against rotenone-induced apoptosis in neuroblastoma cells

Molina-Jiménez, Marı́a Francisca; Sánchez-Reus, Marı́a Isabel; Andrés, David; Cascales, Marı́a; Benedı́, Juana

doi:10.1016/j.brainres.2004.02.065

Cited by 105 publications

(66 citation statements)

References 32 publications

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“…2 0 ,7 0 -Dichlorodihydrofluorescein diacetate (H 2 DCFDA, Wako) is a specific molecular probe for H 2 O 2 , [20][21][22] being diffused through the cell membrane and enzymatically hydrolyzed by intracellular esterases to non-fluorescent dichlorofluorescein which reacts with H 2 O 2 to form a fluorescent compound. HUVECs at 4 Â 10 4 cells/mL were seeded in 24-well plates and preincubated in the HuMedia-EG2 medium for 6 h. After this incubation, the cells were washed once with PBS (À) and fixed for 15 min with 10% formaldehyde at room temperature.…”

Section: )mentioning

confidence: 99%

Increased Monocytic Adhesion by Senescence in Human Umbilical Vein Endothelial Cells

Yanaka

Honma

Sato

et al. 2011

Bioscience, Biotechnology, and Biochemistry

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Section: )mentioning

confidence: 99%

Increased Monocytic Adhesion by Senescence in Human Umbilical Vein Endothelial Cells

Yanaka

Honma

Sato

et al. 2011

Bioscience, Biotechnology, and Biochemistry

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“…Reactive oxygen species (ROS) have been shown as causative factors involved in many human degenerative diseases and antioxidants have been found to have some degree of preventive and therapeutic effects on these disorders 4,5 . Evidence for involvement of free radicals in Alzheimer disease (AD) includes the presence of elevated levels of protein oxidation, lipid peroxidation products and oxidative damage to mitochondria in AD brain 5 .…”

Section: Introductionmentioning

confidence: 99%

“…Evidence for involvement of free radicals in Alzheimer disease (AD) includes the presence of elevated levels of protein oxidation, lipid peroxidation products and oxidative damage to mitochondria in AD brain 5 . Antioxidants protect against the radicals and it is important to balance an enhanced radical production with a sufficient supply of antioxidants 6 .…”

Section: Introductionmentioning

confidence: 99%

Simple chalcones and bis-chalcones ethers as possible pleiotropic agents

Liargkova

Hadjipavlou‐Litina

Koukoulitsa

et al. 2015

Journal of Enzyme Inhibition and Medicinal Chemistry

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The synthesis, the antioxidative properties and the lipoxygenase (LOX) and acetylcholinesterase (AChE) inhibition of a number of 4-hydroxy-chalcones diversely substituted as well as of a series of bis-chalcones ether derivatives are reported. The chalcones derivatives were readily produced using a Claisen-Schmidt condensation in a ultra sound bath in good yields. The structures of the synthesized compounds were confirmed by spectral and elemental analysis. Their lipophilicity is experimentally determined by reversed-phase thin-layer chromatography method. Most of them are potent in vitro inhibitors of lipid peroxidation and of LOX. Compounds b2 and b3 were found to be the most potent LOX and AChE inhibitors among the tested derivatives with a significant anti-lipid peroxidation profile. The results led us to propose these enone derivatives as new multifunctional compounds against Alzheimer's disease. The results are discussed in terms of structural and physicochemical characteristics of the compounds. Moreover, the pharmacokinetic profile of these compounds was investigated using computational methods.

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“…16,47 In addition, in vitro studies have reported that myricetin, at 50 lM, protects neurons against insults induced by neurotoxins. 11,12,48 In this study, myricetin-mediated inhibition of glutamate release is dose dependent, maximal at 70 lM, with a IC 50 of 18 lM. Although the exact mechanism of the neuroprotective activity of myricetin remains to be further clarified, the possible involvement of scavenging free radicals or antioxidant properties has been reported.…”

Section: Discussionmentioning

confidence: 58%

“…[7][8][9] In addition to these properties, numerous studies have demonstrated the neuroprotective effects of myricetin. For example, myricetin attenuates oxidative stress, glutamate, 1-methyl-4-phenylpyridinium, or amyloid-induced neurotoxicity, [10][11][12][13][14][15] and improves cognitive impairment. 16 However, the mechanism(s) involved in these neuroprotective effects are yet to be fully elucidated.…”

Section: Introduction Fmentioning

confidence: 99%

Myricetin Inhibits the Release of Glutamate in Rat Cerebrocortical Nerve Terminals

Chang

Wang

et al. 2015

Journal of Medicinal Food

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The excessive release of glutamate is a critical element in the neuropathology of acute and chronic brain disorders. The purpose of the present study was to investigate the effect and possible mechanism of myricetin, a naturally occurring flavonoid with a neuroprotective profile, on endogenous glutamate release in the nerve terminals (synaptosomes) of the rat cerebral cortex. The release of glutamate was evoked by the K + channel blocker 4-aminopyridine (4-AP) and measured by one-line enzyme-coupled fluorometric assay. We also used a membrane potential-sensitive dye to assay the synaptosomal plasma membrane potential, and a Ca 2 + indicator Fura-2 to monitor cytosolic Ca 2 + concentrations ([Ca 2 + ]C). Results show that myricetin inhibited 4-AP-evoked glutamate release, and this effect was prevented by chelating extracellular Ca 2 + ions and the vesicular transporter inhibitor bafilomycin A1. However, the glutamate transporter inhibitor dl-threo-beta-benzyl-oxyaspartate had no effect on myricetin action. Myricetin did not alter the synaptosomal membrane potential, but decreased 4-APinduced increases in the cytosolic free Ca 2 + concentration. Furthermore, the myricetin effect on 4-AP-evoked glutamate release was prevented by blocking the Cav2.2 (N-type) and Cav2.1 (P/Q-type) channels, but not by blocking intracellular Ca 2 + release. These results suggest that myricetin inhibits glutamate release from cerebrocortical synaptosomes by attenuating voltage-dependent Ca 2 + entry. This implies that the inhibition of glutamate release is an important pharmacological activity of myricetin that may play a critical role in the apparent clinical efficacy of this compound.

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Neuroprotective effect of fraxetin and myricetin against rotenone-induced apoptosis in neuroblastoma cells

Cited by 105 publications

References 32 publications

Increased Monocytic Adhesion by Senescence in Human Umbilical Vein Endothelial Cells

Increased Monocytic Adhesion by Senescence in Human Umbilical Vein Endothelial Cells

Simple chalcones and bis-chalcones ethers as possible pleiotropic agents

Myricetin Inhibits the Release of Glutamate in Rat Cerebrocortical Nerve Terminals

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