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10.3892/ijmm.2016.2701 http://scihub22266oqcxt.onion/10.3892/ijmm.2016.2701 C5029968!5029968!27511125     free     free     free Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Int+J+Mol+Med 2016 ; 38 (4): 1152-60 Nephropedia Template TP {{tp|p=27511125|t=2016. Neuroprotective effects of sodium hydrosulfide against ?-amyloid-induced neurotoxicity |pdf=|usr=}}{{27511125}} gab.com Text Neuroprotective effects of sodium hydrosulfide against -amyloid-induced neurotoxicity JO: Int J Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=27511125 #FOAvip Alzheimer's disease (AD) is known to be caused by the accumulation of amyloid-? peptide (A?). The accumulation of A? has been shown to cause learning and memory impairment in rats, and it has been shown that hydrogen sulfide donors, such as sodium hydrosulfide (NaHS) can attenuate these effects. However, the underlying mechanisms have not yet been fully eludicated. This study was designed to investigate whether NaHS attenuates the inflammation and apoptosis induced by A?. We demonstrated that NaHS attenuated A?25?35-induced neuronal reduction and apoptosis, and inhibited the activation of pro-caspase-3. It also decreased the protein expresion of phosphodiesterase 5 (PDE5) in the hippocampus of the rats. In addition, NaHS upregulated the expression of peroxisome proliferator-activated receptor (PPAR)-? and PPAR-?, but it did not affect the expression of PPAR-?. Moreover, the A?25?35-exposed rats exhibited a decrease in I?B-? degradation and an increase in nuclear factor-?B (NF-?B) p65 phosphorylation levels, whereas these effects were attenuated by NaHS. Our data suggest that NaHS prevents A?-induced neurotoxicity via the upregulation of PPAR-? and PPAR-? and the inhibition of PDE5. Hence NaHS may prove to be beneficial in the treatment of AD. Twit Text FOAVip Neuroprotective effects of sodium hydrosulfide against -amyloid-induced neurotoxicity ????Int J Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=27511125 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27511125 #FOAvip English Wikipedia <ref>{{Cite pmid|27511125}}</ref> Neuroprotective effects of sodium hydrosulfide against ?-amyloid-induced neurotoxicity #MMPMID27511125 Li XH; Deng YY; Li F; Shi JS; Gong QH Int J Mol Med 2016[Oct]; 38 (4): 1152-60 PMID27511125show ga Alzheimer's disease (AD) is known to be caused by the accumulation of amyloid-? peptide (A?). The accumulation of A? has been shown to cause learning and memory impairment in rats, and it has been shown that hydrogen sulfide donors, such as sodium hydrosulfide (NaHS) can attenuate these effects. However, the underlying mechanisms have not yet been fully eludicated. This study was designed to investigate whether NaHS attenuates the inflammation and apoptosis induced by A?. We demonstrated that NaHS attenuated A?25?35-induced neuronal reduction and apoptosis, and inhibited the activation of pro-caspase-3. It also decreased the protein expresion of phosphodiesterase 5 (PDE5) in the hippocampus of the rats. In addition, NaHS upregulated the expression of peroxisome proliferator-activated receptor (PPAR)-? and PPAR-?, but it did not affect the expression of PPAR-?. Moreover, the A?25?35-exposed rats exhibited a decrease in I?B-? degradation and an increase in nuclear factor-?B (NF-?B) p65 phosphorylation levels, whereas these effects were attenuated by NaHS. Our data suggest that NaHS prevents A?-induced neurotoxicity via the upregulation of PPAR-? and PPAR-? and the inhibition of PDE5. Hence NaHS may prove to be beneficial in the treatment of AD. äNeuroprotective effects of sodium hydrosulfide against ?-amyloid-induc(epmc).pdf DeepDyve Pubget Overpricing