JHLT open · 2025
Histidine-rich glycoprotein ameliorated lung ischemia-reperfusion injury in a mouse model.
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Kubo Yujiro, Sugimoto Seiichiro, Ousaka Daiki, Wang Dengli, Ohara Toshiaki, Shiotani Toshio, Tanaka Shin, Suzawa Ken, Shien Kazuhiko, Miyoshi Kentaroh, Okazaki Mikio, Hosono Yasuyuki, Matsukawa Akihiro, Toyooka Shinichi
Аннотация
BACKGROUND: Histidine-rich glycoprotein (HRG) is a multifunctional plasma glycoprotein involved in the regulation of various biological processes. Decreased plasma levels of HRG at 72 h after lung transplantation have been shown to be associated with severe primary graft dysfunction and poor transplant outcomes. In this study, we examined the effect of HRG supplementation on lung ischemia-reperfusion injury (IRI) in mice.
METHODS: The experimental mice were divided into a Sham group and three IRI groups (n=5 each) that received phosphate-buffered saline, human serum albumin, or HRG (HRG/IRI group), respectively. The lung function, lung injury, neutrophil infiltration, cellular apoptosis, inflammatory mediators, neutrophil extracellular traps (NETs), translocation status of high-mobility group box 1 (HMGB1), and hemolytic products in the injured tissue/plasma were compared among the groups.
RESULTS: The HRG/IRI group showed significantly improved oxygenation capacity and a reduced severity of lung injury as compared with the other IRI groups. The HRG/IRI group also showed significantly less severe tissue inflammation in the reperfused lung, including a lower level of neutrophil infiltration, apoptotic cells, and neutrophil-associated inflammatory mediators than the other IRI groups. Moreover, formation of NETs and HMGB1 translocation were significantly suppressed in the HRG/IRI group as compared with the other IRI groups. A significantly greater degree of scavenging of hemolytic products was observed in the HRG/IRI group than the other IRI groups.
CONCLUSION: HRG supplementation ameliorated lung IRI in mice by suppressing inflammatory responses triggered by neutrophil-associated factors, including formation of NETs, HMGB1 translocation, and accumulation of hemolytic products.
METHODS: The experimental mice were divided into a Sham group and three IRI groups (n=5 each) that received phosphate-buffered saline, human serum albumin, or HRG (HRG/IRI group), respectively. The lung function, lung injury, neutrophil infiltration, cellular apoptosis, inflammatory mediators, neutrophil extracellular traps (NETs), translocation status of high-mobility group box 1 (HMGB1), and hemolytic products in the injured tissue/plasma were compared among the groups.
RESULTS: The HRG/IRI group showed significantly improved oxygenation capacity and a reduced severity of lung injury as compared with the other IRI groups. The HRG/IRI group also showed significantly less severe tissue inflammation in the reperfused lung, including a lower level of neutrophil infiltration, apoptotic cells, and neutrophil-associated inflammatory mediators than the other IRI groups. Moreover, formation of NETs and HMGB1 translocation were significantly suppressed in the HRG/IRI group as compared with the other IRI groups. A significantly greater degree of scavenging of hemolytic products was observed in the HRG/IRI group than the other IRI groups.
CONCLUSION: HRG supplementation ameliorated lung IRI in mice by suppressing inflammatory responses triggered by neutrophil-associated factors, including formation of NETs, HMGB1 translocation, and accumulation of hemolytic products.