Tempol, an intracelullar free radical scavenger, reduces liver injury in hepatic ischemia-reperfusion in the rat

2004 ◽  
Vol 36 (4) ◽  
pp. 849-853 ◽  
Author(s):  
B Sepodes ◽  
R Maio ◽  
R Pinto ◽  
C Marques ◽  
J Mendes-do-Vale ◽  
...  
Keyword(s):  
Free Radical ◽  
Liver Injury ◽  
Ischemia Reperfusion ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion

scholarly journals Potential benefits of melatonin in organ transplantation: a review

2016 ◽  
Vol 229 (3) ◽  
pp. R129-R146 ◽  
Author(s):  
Eduardo Esteban-Zubero ◽  
Francisco Agustín García-Gil ◽  
Laura López-Pingarrón ◽  
Moisés Alejandro Alatorre-Jiménez ◽  
Pablo Iñigo-Gil ◽  
...  
Keyword(s):  
Free Radical ◽  
Organ Transplantation ◽  
Graft Rejection ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Antioxidant Defense System ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Therapeutic Tool ◽  
Term Survival

Organ transplantation is a useful therapeutic tool for patients with end-stage organ failure; however, graft rejection is a major obstacle in terms of a successful treatment. Rejection is usually a consequence of a complex immunological and nonimmunological antigen-independent cascade of events, including free radical-mediated ischemia-reperfusion injury (IRI). To reduce the frequency of this outcome, continuing improvements in the efficacy of antirejection drugs are a top priority to enhance the long-term survival of transplant recipients. Melatonin (N-acetyl-5-methoxytryptamine) is a powerful antioxidant and ant-inflammatory agent synthesized from the essential amino acid l-tryptophan; it is produced by the pineal gland as well as by many other organs including ovary, testes, bone marrow, gut, placenta, and liver. Melatonin has proven to be a potentially useful therapeutic tool in the reduction of graft rejection. Its benefits are based on its direct actions as a free radical scavenger as well as its indirect antioxidative actions in the stimulation of the cellular antioxidant defense system. Moreover, it has significant anti-inflammatory activity. Melatonin has been found to improve the beneficial effects of preservation fluids when they are enriched with the indoleamine. This article reviews the experimental evidence that melatonin is useful in reducing graft failure, especially in cardiac, bone, otolaryngology, ovarian, testicular, lung, pancreas, kidney, and liver transplantation.

Matrine attenuates endotoxin-induced acute liver injury after hepatic ischemia/reperfusion in rats

Surgery Today ◽  
2011 ◽  
Vol 41 (8) ◽  
pp. 1075-1084 ◽  
Author(s):  
Feng Zhang ◽  
Xun Wang ◽  
Liquan Tong ◽  
Haiquan Qiao ◽  
Xinlei Li ◽  
...  
Keyword(s):  
Liver Injury ◽  
Acute Liver Injury ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion

scholarly journals WNT AGONIST ATTENUATES LIVER INJURY AND IMPROVES SURVIVAL AFTER HEPATIC ISCHEMIA/REPERFUSION

Shock ◽  
2013 ◽  
Vol 39 (1) ◽  
pp. 3-10 ◽  
Author(s):  
Michael Kuncewitch ◽  
Weng-Lang Yang ◽  
Ernesto Molmenti ◽  
Jeffrey Nicastro ◽  
Gene F. Coppa ◽  
...  
Keyword(s):  
Liver Injury ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion

scholarly journals Acidic Microenvironment Aggravates the Severity of Hepatic Ischemia/Reperfusion Injury by Modulating M1-Polarization Through Regulating PPAR-γ Signal

2021 ◽  
Vol 12 ◽  
Author(s):  
Wei Ding ◽  
Yunfei Duan ◽  
Zhen Qu ◽  
Jiawei Feng ◽  
Rongsheng Zhang ◽  
...  
Keyword(s):  
Liver Injury ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Acidic Microenvironment ◽  
Ppar Γ ◽  
M1 Polarization ◽  
Hepatic Ischemia Reperfusion

Hepatic injury induced by ischemia and reperfusion (HIRI) is a major clinical problem after liver resection or transplantation. The polarization of macrophages plays an important role in regulating the severity of hepatic ischemia/reperfusion injury. Recent evidence had indicated that the ischemia induces an acidic microenvironment by causing increased anaerobic glycolysis and accumulation of lactic acid. We hypothesize that the acidic microenvironment might cause the imbalance of intrahepatic immunity which aggravated HIRI. The hepatic ischemia/reperfusion injury model was established to investigate the effect of the acidic microenvironment to liver injury. Liposomes were used to deplete macrophages in vivo. Macrophages were cultured under low pH conditions to analyze the polarization of macrophages in vitro. Activation of the PPAR-γ signal was determined by Western blot. PPAR-γ agonist GW1929 was administrated to functionally test the role of PPAR-γ in regulating macrophage-mediated effects in the acidic microenvironment during HIRI. We demonstrate that acidic microenvironment aggravated HIRI while NaHCO3 reduced liver injury through neutralizing the acid, besides, liposome abolished the protective ability of NaHCO3 through depleting the macrophages. In vivo and vitro experiment showed that acidic microenvironment markedly promoted M1 polarization but inhibited M2 polarization of macrophage. Furthermore, the mechanistic study proved that the PPAR-γ signal was suppressed during the polarization of macrophages under pH = 6.5 culture media. The addition of PPAR-γ agonist GW1929 inhibited M1 polarization under acidic environment and reduced HIRI. Our results indicate that acidic microenvironment is a key regulator in HIRI which promoted M1 polarization of macrophages through regulating PPAR-γ. Conversely, PPAR-γ activation reduced liver injury, which provides a novel therapeutic concept to prevent HIRI.

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