Amy A Bravo; Krneta Kumm; Catalina Lamy; Jorge Jeanneau; Gisèle Cuello; Jack Lefer
Abstract
Sepsis involves a robust inflammatory response, involving up-regulated chemokine expression and leukocyte accumulation, contributes to the mechanism of myocardial injury and cardiac dysfunction. Currently, it is unknown whether H2 suppresses myocardial inflammatory response to sepsis. We tested the hypothesis that treated mouse by H2 protects the heart against sepsis and LV dysfunction through suppression of the high-mobility group box 1 protein (HMGB1) expression. Cecal ligation and puncture (CLP) was used to induce sepsis. By inhaled mice with 2% H2 for 1 h followed CLP in both sham and sepsis model mice was associated with reduced myocardial cell injury mainly associated with reduced expression of HMGB1. Furthermore, H2 treated animals associated with decreased numbers of monocyte and improved LV function. These findings suggest that this novel H2 has a therapeutic potential for the regulation of myocardial inflammatory response to sepsis.
Keywords: Sepsis; Hydrogen; Inflammatory response; HMGB1; CLP
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