Effects Of Exogenous Hydrogen Sulfide On Redox Equilibrium Of Septic Macrophages

Sepsis is a life-threatening organ dysfunction caused by the host's imbalance of response to infection.It includes many serious complications from clinical critical patients.Sepsis can progress to severe sepsis,and septic shock eventually leads to death.Various mechanisms are involved in the occurrence and development of sepsis.Oxidative stress,as a major cause of sepsis and septic shock,has been the research focus in recent years.Objective:To explore the effects of exogenous Hydrogen Sulfide?H₂S?on redox balance of macrophages in sepsis.Method:Five groups were established according to the different co-cultured reagents with the macrophage strain J774:Grorp A:Phosphate Buffer Saline?PBS??1ml/ml?,GrorpB:Lipopolysaccharide?LPS??1?g/ml?,GrorpC:DL-Propargylglycine?PAG??1mmol/L?+LPS?1?g/ml?,Grorp D:GYY4137?500?mol/L?--H₂S donor,Grorp E:GYY4137?500?mol/L?+LPS?1?g/ml?.In the supernatant of cell culture of each group,the concentration of reactive oxygen species?ROS?,malondialdehyde?MDA?,superoxide dismutase?SOD?,catalase?CAT?and glutathione peroxidase?GSH-Px?were measured by enzyme linked immunosorbent assay?ELISA?.The changes of mitochondrial morphology in cells were observed by electron microscope.Results:The concentration of ROS,MDA,SOD,CAT and GSH-Px in the group B were 90.293±0.217IU/ml,1.665±0.068nmol/m,89.857±3.002U/ml,8.099±0.130U/ml and 10.287±0.335?mol/L,respectively.The concentration of ROS,MDA,SOD,CAT and GSH-Px in the group E were 25.819±2.988IU/ml,0.355±0.065nmol/ml,189.690±0.290U/ml,189.690±0.290U/ml and 287.235±0.864?mol/L,respectively.The concentration of ROS and MDA in the group E were significantly lower than those in the group B?P<0.01?.However,the concentration of SOD,CAT and GSH-Px in the group E were significantly higher than those in the group B?P<0.01?.The damage of cells and mitochondria in group E were slighter than that in group B.Conclusions:H₂S played the protective role on the redox balance of septic macrophages,which may be due to direct inhibited effect of mitochondrial oxidative stress.