The Experts below are selected from a list of 55428 Experts worldwide ranked by ideXlab platform
Hocheol Kim - One of the best experts on this subject based on the ideXlab platform.
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Neuroprotective Effect of tyrosol on transient focal cerebral ischemia in rats
Neuroscience Letters, 2007Co-Authors: Youngmi U, Seongjoo Rho, Jinmo Kim, Miyeo Kim, Dae Hee Lee, Hoyoung Choi, Hocheol Kim, Sun Yeou KimAbstract:Tyrosol (2-(4-hydroxyphenyl)ethanol) is a well-known phenolic compound with antioxidant properties that is present in wine, olive oil, and other plant-derived products. The purpose of this study was to determine the Neuroprotective Effect of tyrosol in a stroke animal model. By using the transient middle cerebral artery occlusion rat model (2 h of occlusion, 22 h of reperfusion), we investigated the Effects of tyrosol on infarct volume and sensory motor function deficit by performing 2,3,5-triphenyltetrazolium chloride staining and behavior tests after ischemia. Tyrosol showed a dose-dependent Neuroprotective Effect that peaked at 64.9% in rats treated with 30 mg/kg of tyrosol. In rotarod, beam balance, and foot fault tests, tyrosol exhibited protective Effects against the sensory motor dysfunction. In conclusion, our results suggest that tyrosol is an appropriate candidate to be used in stroke therapy.
Rafael Franco - One of the best experts on this subject based on the ideXlab platform.
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Neuroprotective Effect of JZL184 in MPP(+)-Treated SH-SY5Y Cells Through CB2 Receptors.
Molecular neurobiology, 2015Co-Authors: María S. Aymerich, Estefanía Rojo-bustamante, Carmen Molina, Marta Celorrio, Juan A. Sánchez-arias, Rafael FrancoAbstract:Growing evidence suggests that the endocannabinoid system plays a role in neuroprotection in Parkinson’s disease. Recently, we have shown the Neuroprotective Effect of monoacylglycerol lipase (MAGL) inhibition with JZL184 in the chronic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model. However, further investigation is needed to determine the Neuroprotective mechanisms of the endocannabinoid system on the nigrostriatal pathway. The aim of this work was to investigate whether the Neuroprotective Effect of JZL184 in mice could be extended to an in vitro cellular model to further understand the mechanism of action of the drug. The SH-SY5Y cell line was selected based on its dopaminergic-like phenotype and its susceptibility to 1-methyl-4-phenylpyridinium iodide (MPP+) toxicity. Furthermore, SH-SY5Y cells express both cannabinoid receptors, CB1 and CB2. The present study describes the Neuroprotective Effect of MAGL inhibition with JZL184 in SH-SY5Y cells treated with MPP+. The Effect of JZL184 in cell survival was blocked by AM630, a CB2 receptor antagonist, and it was mimicked with JWH133, a CB2 receptor agonist. Rimonabant, a CB1 receptor antagonist, did not affect JZL184-induced cell survival. These results demonstrate that the Neuroprotective Effect of MAGL inhibition with JZL184 described in animal models of Parkinson’s disease could be extended to in vitro models such as SH-SY5Y cells treated with MPP+. This represents a useful tool to study mechanisms of neuroprotection mediated by MAGL inhibition, and we provide evidence for the possible involvement of CB2 receptors in the improvement of cell survival.
David A Greenberg - One of the best experts on this subject based on the ideXlab platform.
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vascular endothelial growth factor direct Neuroprotective Effect in in vitro ischemia
Proceedings of the National Academy of Sciences of the United States of America, 2000Co-Authors: Kunlin Jin, Xiao Ou Mao, David A GreenbergAbstract:Vascular endothelial growth factor (VEGF) is a hypoxia-inducible angiogenic peptide with recently identified neurotrophic Effects. Because some neurotrophic factors can protect neurons from hypoxic or ischemic injury, we investigated the possibility that VEGF has similar Neuroprotective properties. In HN33, an immortalized hippocampal neuronal cell line, VEGF reduced cell death associated with an in vitro model of cerebral ischemia: at a maximally Effective concentration of 50 ng/ml, VEGF approximately doubled the number of cells surviving after 24 h of hypoxia and glucose deprivation. To investigate the mechanism of neuroprotection by VEGF, the expression of known target receptors for VEGF was measured by Western blotting, which showed that HN33 cells expressed VEGFR-2 receptors and neuropilin-1, but not VEGFR-1 receptors. The neuropilin-1 ligand placenta growth factor-2 failed to reproduce the protective Effect of VEGF, pointing to VEGFR-2 as the site of VEGF's Neuroprotective action. Two phosphatidylinositol 3′-kinase inhibitors, wortmannin and LY294002, reversed the Neuroprotective Effect of VEGF, implicating the phosphatidylinositol 3′-kinase/Akt signal transduction system in VEGF-mediated neuroprotection. VEGF also protected primary cultures of rat cerebral cortical neurons from hypoxia and glucose deprivation. We conclude that in addition to its known role as an angiogenic factor, VEGF may exert a direct Neuroprotective Effect in hypoxic-ischemic injury.
Nobuaki Egashira - One of the best experts on this subject based on the ideXlab platform.
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Involvement of GABAA Receptors in the Neuroprotective Effect of Theanine on Focal Cerebral Ischemia in Mice
Journal of pharmacological sciences, 2007Co-Authors: Nobuaki Egashira, Kazuhide Hayakawa, Megumi Osajima, Kenichi Mishima, Katsunori Iwasaki, Ryozo Oishi, Michihiro FujiwaraAbstract:We investigated the involvement of gamma-aminobutyric acid(A) (GABA(A)) receptors in the Neuroprotective Effect of gamma-glutamylethylamide (theanine), a component of Japanese green tea, following a 4-h middle cerebral artery (MCA) occlusion in mice. Theanine (1 mg/kg) reduced the size of the cerebral infarct and alterations of NeuN, GFAP, and Iba 1 expression levels at 24 h after MCA occlusion. This Neuroprotective Effect of theanine was prevented by bicuculline (GABA(A)-receptor antagonist, 10 mg/kg) but not 3-mercaptopropionic acid (glutamate decarboxylase inhibitor). These results suggest that the Neuroprotective Effect of theanine is mediated, at least in part, by GABA(A) receptors.
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Repeated treatment with cannabidiol but not Δ9-tetrahydrocannabinol has a Neuroprotective Effect without the development of tolerance
Neuropharmacology, 2007Co-Authors: Kazuhide Hayakawa, Kenichi Mishima, Masanori Nozako, Ayumi Ogata, Mai Hazekawa, An Xin Liu, Masayuki Fujioka, Kohji Abe, Nobuyoshi Hasebe, Nobuaki EgashiraAbstract:Abstract Both Δ9-tetrahydrocannabinol (Δ9-THC) and cannabidiol are known to have a Neuroprotective Effect against cerebral ischemia. We examined whether repeated treatment with both drugs led to tolerance of their Neuroprotective Effects in mice subjected to 4 h-middle cerebral artery (MCA) occlusion. The Neuroprotective Effect of Δ9-THC but not cannabidiol was inhibited by SR141716, cannabinoid CB1 receptor antagonist. Fourteen-day repeated treatment with Δ9-THC, but not cannabidiol, led to tolerance of the Neuroprotective and hypothermic Effects. In addition, repeated treatment with Δ9-THC reversed the increase in cerebral blood flow (CBF), while cannabidiol did not reverse that Effect. Repeated treatment with Δ9-THC caused CB1 receptor desensitization and down-regulation in MCA occluded mice. On the contrary, cannabidiol did not influence these Effects. Moreover, the Neuroprotective Effect and an increase in CBF induced by repeated treatment with cannabidiol were in part inhibited by WAY100135, serotonin 5-HT1A receptor antagonist. Cannabidiol exhibited stronger antioxidative power than Δ9-THC in an in vitro study using the 1,1-diphenyl-2-picryhydrazyl (DPPH) radical. Thus, cannabidiol is a potent antioxidant agent without developing tolerance to its Neuroprotective Effect, acting through a CB1 receptor-independent mechanism. It is to be hoped that cannabidiol will have a palliative action and open new therapeutic possibilities for treating cerebrovascular disorders.
María S. Aymerich - One of the best experts on this subject based on the ideXlab platform.
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Neuroprotective Effect of JZL184 in MPP(+)-Treated SH-SY5Y Cells Through CB2 Receptors.
Molecular neurobiology, 2015Co-Authors: María S. Aymerich, Estefanía Rojo-bustamante, Carmen Molina, Marta Celorrio, Juan A. Sánchez-arias, Rafael FrancoAbstract:Growing evidence suggests that the endocannabinoid system plays a role in neuroprotection in Parkinson’s disease. Recently, we have shown the Neuroprotective Effect of monoacylglycerol lipase (MAGL) inhibition with JZL184 in the chronic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model. However, further investigation is needed to determine the Neuroprotective mechanisms of the endocannabinoid system on the nigrostriatal pathway. The aim of this work was to investigate whether the Neuroprotective Effect of JZL184 in mice could be extended to an in vitro cellular model to further understand the mechanism of action of the drug. The SH-SY5Y cell line was selected based on its dopaminergic-like phenotype and its susceptibility to 1-methyl-4-phenylpyridinium iodide (MPP+) toxicity. Furthermore, SH-SY5Y cells express both cannabinoid receptors, CB1 and CB2. The present study describes the Neuroprotective Effect of MAGL inhibition with JZL184 in SH-SY5Y cells treated with MPP+. The Effect of JZL184 in cell survival was blocked by AM630, a CB2 receptor antagonist, and it was mimicked with JWH133, a CB2 receptor agonist. Rimonabant, a CB1 receptor antagonist, did not affect JZL184-induced cell survival. These results demonstrate that the Neuroprotective Effect of MAGL inhibition with JZL184 described in animal models of Parkinson’s disease could be extended to in vitro models such as SH-SY5Y cells treated with MPP+. This represents a useful tool to study mechanisms of neuroprotection mediated by MAGL inhibition, and we provide evidence for the possible involvement of CB2 receptors in the improvement of cell survival.