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General Health & Fitness
Health Span Extension Research
Anti-Aging & weight-loss effects of Rapamycin
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<blockquote data-quote="SoCal Guy" data-source="post: 77512" data-attributes="member: 14529"><p><strong>Rapamycin Reduces Neurological Deficits after Transient Global Ischemia</strong></p><p></p><p><strong><a href="https://www.ncbi.nlm.nih.gov/pubmed/28729914" target="_blank">Effects of mTOR on Neurological Deficits after Transient Global Ischemia</a></strong>https://www.ncbi.nlm.nih.gov/pubmed/28729914</p><p></p><p><span style="color: #000000"><span style="font-family: 'Arial'">Mammalian target of </span></span><span style="color: #000000"><span style="font-family: 'Arial'">rapamycin</span></span><span style="color: #000000"><span style="font-family: 'Arial'"> (mTOR) is a serine/threonine protein kinase and activation of its signal pathway plays an important role in regulating protein growth and synthesis as well as cell proliferation and survival. </span></span></p><p><span style="color: #000000"><span style="font-family: 'Arial'"></span></span></p><p><span style="color: #000000"><span style="font-family: 'Arial'">In the present study, we examined the contribution of mTOR and its downstream products to brain injuries and neurological deficiencies after cardiac arrest (CA) induced-transient global ischemia. </span></span></p><p><span style="color: #000000"><span style="font-family: 'Arial'"></span></span></p><p><span style="color: #000000"><span style="font-family: 'Arial'">CA was induced by asphyxia followed by cardiopulmonary resuscitation (CPR) in rats. Our results showed that expression of p-mTOR, mTOR-mediated phosphorylation of 4E-binding protein 4 (4E-BP1) and p70 ribosomal S6 protein kinase 1 (S6K1) pathways were amplified in CA rats compared to their controls. </span></span></p><p><span style="color: #000000"><span style="font-family: 'Arial'"></span></span></p><p><span style="color: #000000"><span style="font-family: 'Arial'">Blocking mTOR using </span></span><span style="color: #000000"><span style="font-family: 'Arial'">rapamycin</span></span><span style="color: #000000"><span style="font-family: 'Arial'"> attenuated upregulation of pro-inflammatory cytokines (namely IL-1&#946;, IL-6 and TNF-&#945<img src="data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7" class="smilie smilie--sprite smilie--sprite2" alt=";)" title="Wink ;)" loading="lazy" data-shortname=";)" />, and Caspase-3, indicating cell apoptosis and also promoting the levels of vascular endothelial growth factor (VEGF) and its subtype receptor VEGFR-2 in the hippocampus. Moreover, the effects of </span></span><span style="color: #000000"><span style="font-family: 'Arial'">rapamycin</span></span><span style="color: #000000"><span style="font-family: 'Arial'"> were linked to improvement of neurological deficits and increased brain water content observed in CA rats. </span></span></p><p><span style="color: #000000"><span style="font-family: 'Arial'"></span></span></p><p><span style="color: #000000"><span style="font-family: 'Arial'">In conclusion, activation of mTOR signal is engaged in pathophysiological process during CA-induced transient global ischemia and blocking mTOR pathway plays a beneficial role in regulating injured neuronal tissues and neurological deficits via PIC, apoptotic Caspase-3 and VEGF mechanisms. Targeting one or more of these specific mTOR pathways and its downstream signaling molecules may present new opportunities for neural dysfunction and vulnerability related to transient global ischemia.</span></span></p></blockquote><p></p>
[QUOTE="SoCal Guy, post: 77512, member: 14529"] [b]Rapamycin Reduces Neurological Deficits after Transient Global Ischemia[/b] [b][URL="https://www.ncbi.nlm.nih.gov/pubmed/28729914"]Effects of mTOR on Neurological Deficits after Transient Global Ischemia[/URL][/b]https://www.ncbi.nlm.nih.gov/pubmed/28729914 [COLOR=#000000][FONT=arial]Mammalian target of [/FONT][/COLOR][COLOR=#000000][FONT=arial]rapamycin[/FONT][/COLOR][COLOR=#000000][FONT=arial] (mTOR) is a serine/threonine protein kinase and activation of its signal pathway plays an important role in regulating protein growth and synthesis as well as cell proliferation and survival. In the present study, we examined the contribution of mTOR and its downstream products to brain injuries and neurological deficiencies after cardiac arrest (CA) induced-transient global ischemia. CA was induced by asphyxia followed by cardiopulmonary resuscitation (CPR) in rats. Our results showed that expression of p-mTOR, mTOR-mediated phosphorylation of 4E-binding protein 4 (4E-BP1) and p70 ribosomal S6 protein kinase 1 (S6K1) pathways were amplified in CA rats compared to their controls. Blocking mTOR using [/FONT][/COLOR][COLOR=#000000][FONT=arial]rapamycin[/FONT][/COLOR][COLOR=#000000][FONT=arial] attenuated upregulation of pro-inflammatory cytokines (namely IL-1β, IL-6 and TNF-α), and Caspase-3, indicating cell apoptosis and also promoting the levels of vascular endothelial growth factor (VEGF) and its subtype receptor VEGFR-2 in the hippocampus. Moreover, the effects of [/FONT][/COLOR][COLOR=#000000][FONT=arial]rapamycin[/FONT][/COLOR][COLOR=#000000][FONT=arial] were linked to improvement of neurological deficits and increased brain water content observed in CA rats. In conclusion, activation of mTOR signal is engaged in pathophysiological process during CA-induced transient global ischemia and blocking mTOR pathway plays a beneficial role in regulating injured neuronal tissues and neurological deficits via PIC, apoptotic Caspase-3 and VEGF mechanisms. Targeting one or more of these specific mTOR pathways and its downstream signaling molecules may present new opportunities for neural dysfunction and vulnerability related to transient global ischemia.[/FONT][/COLOR] [/QUOTE]
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Anti-Aging & weight-loss effects of Rapamycin
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