Neurochemical research
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Neurochemical research · Mar 2012
Neuroprotective effect of sesame seed oil in 6-hydroxydopamine induced neurotoxicity in mice model: cellular, biochemical and neurochemical evidence.
Natural antioxidants have shown a remarkable reduction in oxidative stress due to excess formation of reactive oxygen species by enhancing antioxidant mechanism in the neurodegenerative disorders. Sesame seed oil (SO) is one of the most important edible oil in India as well as in Asian countries and has potent antioxidant properties thus the present study evaluated the neuroprotective effect of SO by using 6-Hydroxydopamine (6-OHDA)-induced Parkinson's disease model in mice. The mice were fed an SO mix diet for 15 days and then 6-OHDA was injected into the right striatum of mice brain. ⋯ The pretreatment of SO on antioxidant mechanism and dopamine level in the brain had shown some significant improvement in Lesion+SO (L+SO) group when compared with Lesioned group. However, NADPH oxidase subunit, Nox2 and inflammatory stimulator Cox2 expression was increased as well as antioxidant MnSOD level was decreased in Lesioned group while SO showed the inhibitory effect on the activation of Nox2 and Cox2 and restored MnSOD expression in L+SO group. Increased tyrosine hydroxylase (TH) expression in substantia nigra as well as dopamine and its metabolite DOPAC level in L+SO group also support our findings that SO may inhibit activation of NADPH oxidase dependent inflammatory mechanism due to 6-OHDA induced neurotoxicity in mice.
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Neurochemical research · Feb 2012
Mechanisms of VEGF- and glutamate-induced inhibition of osmotic swelling of murine retinal glial (Müller) cells: indications for the involvement of vesicular glutamate release and connexin-mediated ATP release.
We determined the mechanisms of glutamate and ATP release from murine retinal glial (Müller) cells by pharmacological manipulation of the vascular endothelial growth factor (VEGF)- and glutamate-induced inhibition of cellular swelling under hypoosmotic conditions. It has been shown that exogenous glutamate inhibits hypoosmotic swelling of rat Müller cells via the induction of the release of ATP (Uckermann et al. in J Neurosci Res 83:538-550, 53). VEGF was shown to inhibit hypoosmotic swelling of rat Müller cells by inducing the release of glutamate (Wurm et al. in J Neurochem 104:386-399, 55). ⋯ The effects of both VEGF and glutamate were blocked by tetrodotoxin and by an inhibitor of T-type voltage-gated calcium channels. Murine Müller cells display connexin-43 immunoreactivity. The data suggest that Müller cells of the murine retina may release glutamate by vesicular exocytosis, whereas ATP is released through connexin hemichannels.
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Neurochemical research · Feb 2012
L-type calcium channel mediates anticonvulsant effect of cannabinoids in acute and chronic murine models of seizure.
The anticonvulsant activities of cannabinoid compounds have been shown in various models of seizure and epilepsy. At least, part of antiseizure effects of cannabinoid compounds is mediated through calcium (Ca(2+)) channels. The L-type Ca(2+) channels have been shown to be important in various epilepsy models. ⋯ Moreover, (R)-(+)-[2,3-dihydro-5-methyl-3[(4-morpholinyl)methyl]pyrrolo[1,2,3-de]-1,4-benzoxazinyl]-(1-naphthalenyl) methanone mesylate (WIN55,212-2), the non-selective cannabinoid CB1 and CB2 receptor agonist showed anticonvulsant effect in amygdala-kindled rats. However, co-administration of WIN55,212-2 and verapamil attenuated the protective properties of WIN55,212-2. Our results showed that the anticonvulsant activity of cannabinoid compounds is mediated, at least in part, by L-type Ca(2+) channels in these two models of convulsion and epilepsy.
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Neurochemical research · Feb 2012
Effects of antagonists and heat on TRPM8 channel currents in dorsal root ganglion neuron activated by nociceptive cold stress and menthol.
Transient receptor potential ion channel melastatin subtype 8 (TRPM8) is activated by cold temperature and cooling agents, such as menthol and icilin. Compounds containing peppermint are reported to reduce symptoms of environmental cold stress such as cold allodynia in dorsal root ganglion (DRG) neuron; however, the underlying mechanisms of action are unclear. We tested the effects of physiological heat (37°C), anthralic acid (ACA and 0.025 mM), 2-aminoethyl diphenylborinate (2-APB and 0.05) on noxious cold (10°C) and menthol (0.1 mM)-induced TRPM8 cation channel currents in the DRG neurons of rats. ⋯ Noxious cold-induced Ca(2+) gates were blocked by the ACA although menthol-induced TRPM8 currents were not blocked by ACA and 2-APB. In conclusion, the results suggested that activation of TRPM8 either by menthol or nociceptive cold can activate TRPM8 channels although we observed the protective role of heat, ACA and 2-APB through a TRPM8 channel in nociceptive cold-activated DRG neurons. Since cold allodynia is a common feature of neuropathic pain and diseases of sensory neuron, our findings are relevant to the etiology of neuropathology in DRG neurons.
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Neurochemical research · Dec 2011
Resveratrol pretreatment attenuates cerebral ischemic injury by upregulating expression of transcription factor Nrf2 and HO-1 in rats.
Oxidative stress damage plays a vital role in cerebral ischemia/reperfusion (I/R) pathogenesis. The nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway can be activated by pharmacological and dietary means to attenuate cellular oxidative stress. Resveratrol, a plant-derived polyphenolic compound, has antioxidant property. ⋯ These results showed that resveratrol pretreatment had neuroprotective effects on cerebral I/R injury. This neuroprotective effect is likely exerted by upregulated expression of transcription factor Nrf2 and HO-1 to ameliorate oxidative damage, decreased the protein expression of caspase-3. Our finding is important for understanding the neuroprotective mechanism of resveratrol and promoting its clinical therapeutic utility.