ObjectiveTo study the effects of hydrogen sulfide (H2S) on myocardial injury in sepsis rats, and to explore the possible mechanism of H2S on myocardial injury induced by sepsis.MethodsCecal ligation and puncture (CLP) method was used to establish sepsis rat model. SD rats were randomly divided into 6 groups:sham operation group, sham operation + exogenous H2S donor sodium thiohydride group, pseudosurgery +H2S synthase cthioether-ether lyase (cystathionine-γ-lyase, CSE) inhibitor propargylglycine (propargylglycine, PAG) group, CLP model group, CLP model +NaHS group, CLP model +PAG group, 24 rats in each group. Blood and myocardial specimens were collected from the subgroups of COP for 6 h, 12 h and 24 h, respectively. Serum myocardial calcitonin I (cTnI) level, TNF-α, IL-10 were detected, and the pathological changes were observed by HE staining of rat myocardial tissue. The expression ofCSEmRNA in cardiomyocytes was detected by RT-PCR, Western blot assay was used to detect the expression of cardiac transcription factor NF-κB in rats.ResultsThere was no statistically significant difference in each group and time point of sham operation groups. Compared to the sham 12 h, 24 h group, the concentration of cTnI in serum, and pathological scores of myocardial tissue increased gradually (PCSEmRNA and the level of IL-10 increased (PPCSEmRNA and the level of IL-10 increased (PConclusionH2S plays a protective role in sepsis-induced myocardial injury, and the possible mechanism of this protective effect maybe by inhibiting the expression of NF-κB, reducing the content of TNF-α and improving the content of IL-10 in myocardial tissue.
