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10.1155/2020/2961406 http://scihub22266oqcxt.onion/10.1155/2020/2961406 33273998!7683148!33273998     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=33273998&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Oxid+Med+Cell+Longev 2020 ; 2020 (?): 2961406 Nephropedia Template TP {{tp|p=33273998|t=2020. Cardioprotective Effects of Taurisolo(R) in Cardiomyoblast H9c2 Cells under High-Glucose and Trimethylamine N-Oxide Treatment via De Novo Sphingolipid Synthesis |pdf=|usr=}}{{33273998}} gab.com Text Cardioprotective Effects of Taurisolo(R) in Cardiomyoblast H9c2 Cells under High-Glucose and Trimethylamine N-Oxide Treatment via De Novo Sphingolipid Synthesis JO: Oxid Med Cell Longev http://www.kidney.de/pget.php?&tw=1&pmid=33273998 #FOAvip In addition to high plasma glucose, increased levels of trimethylamine N-oxide (TMAO) have been found in obese subjects, where are considered as a novel risk factor for cardiovascular diseases. The present study aimed to investigate the effect of a novel nutraceutical formulation based on grape polyphenols (registered as Taurisolo(R)) in counteracting TMAO- and high glucose (HG)-induced cytotoxicity in cardiomyoblast H9c2 cells. Cell damage was induced with HG (HG-H9c2) and HG+TMAO (THG-H9c2); both experimental cell models were, thus, incubated for 72 h in the presence or absence of Taurisolo(R). It was observed that Taurisolo(R) significantly increased the cell viability and reduced lactate dehydrogenase and aspartate transaminase release in both HG- and THG-H9c2 cells. Additionally, through its antioxidant activity, Taurisolo(R) modulated cell proliferation via ERK activation in THG-H9c2. Furthermore, Taurisolo(R) was able to induce autophagic process via increasing the expression of LC3II, a protein marker involved in formation of autophagosome and ex novo synthesis of sphingomyelin, ceramides, and their metabolites both in HG- and THG-H9c2 cells. Finally, Taurisolo(R) reduced hypertrophy and induced differentiation of HG-H9C2 cells into cardiomyocyte-like cells. These data suggest that Taurisolo(R) counteracts the toxicity induced by TMAO and HG concentrations increasing autophagic process and activating de novo sphingolipid synthesis, resulting in a morphological cell remodeling. In conclusion, our results allow speculating that Taurisolo(R), combined with energy restriction, may represent a useful nutraceutical approach for prevention of cardiomyopathy in obese subjects. Twit Text FOAVip Cardioprotective Effects of Taurisolo(R) in Cardiomyoblast H9c2 Cells under High-Glucose and Trimethylamine N-Oxide Treatment via De Novo Sphingolipid Synthesis ????Oxid Med Cell Longev http://www.kidney.de/pget.php?&tw=1&pmid=33273998 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33273998 #FOAvip English Wikipedia <ref>{{Cite pmid|33273998}}</ref> Cardioprotective Effects of Taurisolo(R) in Cardiomyoblast H9c2 Cells under High-Glucose and Trimethylamine N-Oxide Treatment via De Novo Sphingolipid Synthesis #MMPMID33273998 Lama S; Monda V; Rizzo MR; Dacrema M; Maisto M; Annunziata G; Tenore GC; Novellino E; Stiuso P Oxid Med Cell Longev 2020[]; 2020 (?): 2961406 PMID33273998show ga In addition to high plasma glucose, increased levels of trimethylamine N-oxide (TMAO) have been found in obese subjects, where are considered as a novel risk factor for cardiovascular diseases. The present study aimed to investigate the effect of a novel nutraceutical formulation based on grape polyphenols (registered as Taurisolo(R)) in counteracting TMAO- and high glucose (HG)-induced cytotoxicity in cardiomyoblast H9c2 cells. Cell damage was induced with HG (HG-H9c2) and HG+TMAO (THG-H9c2); both experimental cell models were, thus, incubated for 72 h in the presence or absence of Taurisolo(R). It was observed that Taurisolo(R) significantly increased the cell viability and reduced lactate dehydrogenase and aspartate transaminase release in both HG- and THG-H9c2 cells. Additionally, through its antioxidant activity, Taurisolo(R) modulated cell proliferation via ERK activation in THG-H9c2. Furthermore, Taurisolo(R) was able to induce autophagic process via increasing the expression of LC3II, a protein marker involved in formation of autophagosome and ex novo synthesis of sphingomyelin, ceramides, and their metabolites both in HG- and THG-H9c2 cells. Finally, Taurisolo(R) reduced hypertrophy and induced differentiation of HG-H9C2 cells into cardiomyocyte-like cells. These data suggest that Taurisolo(R) counteracts the toxicity induced by TMAO and HG concentrations increasing autophagic process and activating de novo sphingolipid synthesis, resulting in a morphological cell remodeling. In conclusion, our results allow speculating that Taurisolo(R), combined with energy restriction, may represent a useful nutraceutical approach for prevention of cardiomyopathy in obese subjects. |Animals[MESH] |Cardiotonic Agents/*pharmacology[MESH] |Cell Line[MESH] |Glucose/*pharmacology[MESH] |Methylamines/*pharmacology[MESH] |Myoblasts, Cardiac/*metabolism/pathology[MESH] |Rats[MESH]Cardioprotective Effects of Taurisolo(R) in Cardiomyoblast H9c2 Cells (epmc).pdf DeepDyve Pubget Overpricing