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| 1 | Role of aldehyde dehydrogenase 2 in ischemia reperfusion injury:An update显示文摘Aldehyde dehydrogenase 2(ALDH2) is best known for its critical detoxifying role in liver alcohol metabolism. However, ALDH2 dysfunction is also involved in a wide range of human pathophysiological situations and is associated with complications such as cardiovascular diseases, diabetes mellitus, neurodegenerative diseases and aging. A growing body of research has shown that ALDH2 provides important protection against oxidative stress and the subsequent loading of toxic aldehydes such as 4-hydroxy-2-nonenal and adducts that occur in human diseases, including ischemia reperfusion injury(IRI). There is increasing evidence of its role in IRI pathophysiology in organs such as heart, brain, small intestine and kidney; however, surprisingly few studies have been carried out in the liver, where ALDH2 is found in abundance. This study reviews the role of ALDH2 in modulating the pathways involved in the pathophysiology of IRI associated with oxidative stress, autophagy and apoptosis. Special emphasis is placed on the role of ALDH2 in different organs, on therapeutic 'preconditioning' strategies, and on the use of ALDH2 agonists such as Alda-1, which may become a useful therapeutic tool for preventing the deleterious effects of IRI in organ transplantation. | Arnau Panisello-Roselló Alexandre Lopez Emma Folch-Puy Teresa Carbonell Anabela Rolo Carlos Palmeira René Adam Marc Net Joan Roselló-Catafau | 2018 | World Journal of Gastroenterology2018，24，27： | 6 |
| 2 | Sirtuin 1 in rat orthotopic liver transplantation:An I GL-1 preservation solution approach显示文摘AIM:To investigate the possible involvement of Sirtuin1(SIRT1)in rat orthotopic liver transplantation(OLT),when Institute Georges Lopez 1(IGL-1)preservation solution is enriched with trimetazidine(TMZ).METHODS:Male Sprague-Dawley rats were used as donors and recipients.Livers were stored in IGL-1 preservation solution for 8h at 4℃,and then underwent OLT according to Kamada’s cuff technique without arterialization.In another group,livers were stored in IGL-1 preservation solution supplemented with TMZ,at10-6 mol/L,for 8 h at 4℃and then underwent OLT.Rats were sacrificed 24 h after reperfusion,and liver and plasma samples were collected.Liver injury(transaminase levels),mitochondrial damage(glutamate dehydrogenase activity)oxidative stress(malondialdehyde levels),and nicotinamide adenine dinucleotide(NAD+),the cofactor necessary for SIRT1 activity,were determined by biochemical methods.SIRT1 and its substrates(acFox O1,ac-p53),the precursor of NAD+,nicotinamide phosphoribosyltransferase(NAMPT),as well as the phosphorylation of adenosine monophosphate activated protein kinase(AMPK),p-m TOR,p-p70S6K(direct substrate of m TOR),autophagy parameters(beclin-1,LC3B)and MAP kinases(p-p38 and p-ERK)were determined by Western blot.RESULTS:Liver grafts preserved in IGL-1 solution enriched with TMZ presented reduced liver injury and mitochondrial damage compared with those preservedin IGL-1 solution alone.In addition,livers preserved in IGL-1+TMZ presented reduced levels of oxidative stress.This was consistent with enhanced SIRT1 protein expression and elevated SIRT1 activity,as indicated by decreased acetylation of p53 and Fox O1.The elevated SIRT1 activity in presence of TMZ can be attributed to the enhanced NAMPT protein and NAD+/NADH levels.Up-regulation of SIRT1 was consistent with activation of AMPK and inhibition of phosphorylation of m TOR and its direct substrate(p-p70S6K).As a consequence,autophagy mediators(beclin-1 and LC3B)were overexpressed.Furthermore,MAP kinases were regulated in livers preserved with IGL-1+TMZ,as they were characterized by enhanced p-ERK and decreased p-p38protein expression.CONCLUSION:Our study shows that IGL-1 preservation solution enriched with TMZ protects liver grafts from the IRI associated with OLT,through SIRT1 up-regulation. | Eirini Pantazi Mohamed Amine Zaouali Mohamed Bejaoui Emma Folch-Puy Hassen Ben Abdennebi Ana Teresa Varela Anabela Pinto Rolo Carlos Marques Palmeira Joan Roselló-Catafau | 2015 | World Journal of Gastroenterology2015，21，6： | 5 |
| 3 | Declining NAD + Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging显示文摘 | Ana P. Gomes Nathan L. Price Alvin J.Y. Ling Javid J. Moslehi Magdalene K. Montgomery Luis Rajman James P. White Jo?o S. Teodoro Christiane D. Wrann Basil P. Hubbard Evi M. Mercken Carlos M. Palmeira Rafael de Cabo Anabela P. Rolo Nigel Turner Eric L. Bel | 2013 | Cell2013，，7： | 2 |
| 4 | Mitochondrially mediated synergistic cell killing by bile acids显示文摘 | Anabela P Rolo Carlos M Palmeira Kendall B Wallace | 2002 | BBA - Molecular Basis of Disease2002，，1： | 1 |
| 5 | Mitochondrially-mediated toxicity of bile acids显示文摘 | Carlos M. Palmeira Anabela P. Rolo | 2004 | Toxicology2004，，1： | 1 |
| 6 | Role of oxidative stress in the pathogenesis of nonalcoholic steatohepatitis显示文摘 | Anabela P. Rolo Jo?o S. Teodoro Carlos M. Palmeira | 2011 | Free Radical Biology and Medicine2011，，1： | 1 |
| 7 | Role of oxidative stress in the pathogenesis of nonalcoholic steatohepatitis显示文摘 | Anabela P. Rolo Jo?o S. Teodoro Carlos M. Palmeira | 2011 | Free Radical Biology and Medicine2011，，1： | 1 |
| 8 | Interactions of combined bile acids on hepatocyte viability: cytoprotection or synergism显示文摘 | Anabela P Rolo Carlos M Palmeira Kendall B Wallace | 2002 | Toxicology Letters2002，，3： | 1 |
| 9 | Diabetes and mitochondrial function: Role of hyperglycemia and oxidative stress 显示文摘 | Rolo Anabela P Carlos M | 2006 | Toxicology and Applied Pharmacology2006，212，： | 1 |
| 10 | Diabetes and mitochondrial function: Role of hyperglycemia and oxidative stress显示文摘 | Anabela P. Rolo Carlos M. Palmeira | 2006 | Toxicology and Applied Pharmacology2006，，： | 1 |
| 11 | Losartan activates sirtuin 1 in rat reduced-size orthotopic liver transplantation显示文摘AIM: To investigate a possible association between losartan and sirtuin 1(SIRT1) in reduced-size orthotopic liver transplantation(ROLT) in rats.METHODS: Livers of male Sprague-Dawley rats(200-250 g) were preserved in University of Wisconsin preservation solution for 1 h at 4 ℃ prior to ROLT.In an additional group,an antagonist of angiotensin Ⅱ type 1 receptor(AT1R),losartan,was orally administered(5 mg/kg) 24 h and 1 h before the surgical procedure to both the donors and the recipients.Transaminase(as an indicator of liver injury),SIRT1 activity,and nicotinamide adenine dinucleotide(NAD+,a co-factor necessary for SIRT1 activity) levels were determined by biochemical methods.Protein expression of SIRT1,acetylated Fox O1(ac-Fox O1),NAMPT(the precursor of NAD+),heat shock proteins(HSP70,HO-1) expression,endoplasmic reticulum stress(GRP78,IRE1 a,p-e IF2) and apoptosis(caspase 12 and caspase 3) parameters were determined by Western blot.Possible alterations in protein expression of mitogen activated protein kinases(MAPK),such as p-p38 and p-ERK,were also evaluated.Furthermore,the SIRT3 protein expression and m RNA levels were examined.RESULTS: The present study demonstrated that losartan administration led to diminished liver injury when compared to ROLT group,as evidenced by the significant decreases in alanine aminotransferase(358.3 ± 133.44 vs 206 ± 33.61,P < 0.05) and aspartate aminotransferase levels(893.57 ± 397.69 vs 500.85 ± 118.07,P < 0.05).The lessened hepatic injury in case of losartan was associated with enhanced SIRT1 protein expression and activity(5.27 ± 0.32 vs 6.08 ± 0.30,P < 0.05).This was concomitant with increased levels of NAD+(0.87 ± 0.22 vs 1.195 ± 0.144,P < 0.05) the co-factor necessary for SIRT1 activity,as well as with decreases in ac-Fox O1 expression.Losartan treatment also provoked significant attenuation of endoplasmic reticulum stress parameters(GRP78,IRE1 a,p-e IF2) which was consistent with reduced levels of both caspase 12 and caspase 3.Furthermore,losartan administration stimulated HSP70 protein expression and attenuated HO-1 expression.However,no changes were observed in protein or m RNA expression of SIRT3.Finally,the protein expression pattern of p-ERK and p-p38 were not altered upon losartan administration.CONCLUSION: The present study reports that losartan induces SIRT1 expression and activity,and that it reduces hepatic injury in a ROLT model. | Eirini Pantazi Mohamed Bejaoui Mohamed Amine Zaouali Emma Folch-Puy Anabela Pinto Rolo Arnau Panisello Carlos Marques Palmeira Joan Roselló-Catafau | 2015 | World Journal of Gastroenterology2015，21，26： | 0 |
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