BACKGROUND AND AIM: Heme oxygenase-1 (HO-1) acts as a protector against hepatic inflammatory injury. HO-1 catalyzes the conversion of heme protein to biliverdin, free iron, and carbon monoxide. Pro-inflammatory responses play critical roles in hepatic ischemia-reperfusion (I/R) injury, and carbon monoxide effectively downregulates I/R injury. The aim of this study was to evaluate the mechanism by which HO-1 reduces warm I/R injury. METHODS: Sprague-Dawley rats were divided into two groups: the 20-min ischemia group (control group; n = 6) and the 20-min ischemia with cobalt protoporphyrin (CoPP group; n = 6). CoPP is an inducer of HO-1 in the sinusoids. Kupffer cells were labeled using the liposome entrapment method, and platelets were labeled with rhodamine-6G. The adherent platelets were observed for up to 120 min after reperfusion by intravital microscopy. RESULTS: In the control group, the number of adherent platelets significantly increased than in the CoPP group. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling-positive cells were observed after 120 min of reperfusion in the control group. They were not observed in the CoPP group. In the CoPP group, serum alanine transaminase and interleukin-6 levels reduced after reperfusion. Moreover, the flow velocity of platelets in the hepatic sinusoid markedly increased. CONCLUSIONS: This study suggests that HO-1 inhibits platelet adhesion to sinusoids. Such inhibition leads to the prevention of hepatic I/R injury.
BACKGROUND AND AIM: Heme oxygenase-1 (HO-1) acts as a protector against hepatic inflammatory injury. HO-1 catalyzes the conversion of heme protein to biliverdin, free iron, and carbon monoxide. Pro-inflammatory responses play critical roles in hepatic ischemia-reperfusion (I/R) injury, and carbon monoxide effectively downregulates I/R injury. The aim of this study was to evaluate the mechanism by which HO-1 reduces warm I/R injury. METHODS:Sprague-Dawley rats were divided into two groups: the 20-min ischemia group (control group; n = 6) and the 20-min ischemia with cobalt protoporphyrin (CoPP group; n = 6). CoPP is an inducer of HO-1 in the sinusoids. Kupffer cells were labeled using the liposome entrapment method, and platelets were labeled with rhodamine-6G. The adherent platelets were observed for up to 120 min after reperfusion by intravital microscopy. RESULTS: In the control group, the number of adherent platelets significantly increased than in the CoPP group. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling-positive cells were observed after 120 min of reperfusion in the control group. They were not observed in the CoPP group. In the CoPP group, serum alanine transaminase and interleukin-6 levels reduced after reperfusion. Moreover, the flow velocity of platelets in the hepatic sinusoid markedly increased. CONCLUSIONS: This study suggests that HO-1 inhibits platelet adhesion to sinusoids. Such inhibition leads to the prevention of hepatic I/R injury.
Authors: Kojiro Nakamura; Shoichi Kageyama; Shi Yue; Jing Huang; Takehiro Fujii; Bibo Ke; Rebecca A Sosa; Elaine F Reed; Nakul Datta; Ali Zarrinpar; Ronald W Busuttil; Jerzy W Kupiec-Weglinski Journal: Am J Transplant Date: 2017-12-18 Impact factor: 8.086
Authors: Isaclaudia G de Azevedo-Quintanilha; Isabel M Medeiros-de-Moraes; André C Ferreira; Patrícia A Reis; Adriana Vieira-de-Abreu; Robert A Campbell; Andrew S Weyrich; Patricia T Bozza; Guy A Zimmerman; Hugo C Castro-Faria-Neto Journal: Malar J Date: 2020-07-01 Impact factor: 2.979
Authors: Ivan Linares-Cervantes; Dagmar Kollmann; Toru Goto; Juan Echeverri; Johan Moritz Kaths; Matyas Hamar; Peter Urbanellis; Laura Mazilescu; Roizar Rosales; Claudia Bruguera; Fabiola Oquendo; Sujani Ganesh; Oyedele A Adeyi; Paul Yip; Nazia Selzner; Markus Selzner Journal: Transplant Direct Date: 2019-03-04