[Effect and Mechanism of Hydrogen Sulfide on Septic Rats with Myocardial Injury].

OBJECTIVE

To study the effects of hydrogen sulfide (H2 S) on myocardial injury in sepsis rats, and to explore the possible mechanism of H2 S on myocardial injury induced by sepsis.

METHODS

Cecal 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 H2 S donor sodium thiohydride group, pseudosurgery +H2 S 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 of CSE mRNA in cardiomyocytes was detected by RT-PCR, Western blot assay was used to detect the expression of cardiac transcription factor NF-κB in rats.

RESULTS

There 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 (P<0.05) in the CLP 12 h and 24 h group. Compared to the CLP 12 h, 24 h group, in the CLP + NaHS 12 h, 24 h group, the concentration of cTnI in serum, and pathological scores of myocardial tissue, the expression of NF-κB, the level of TNF-α decreased and the expression of CSE mRNA and the level of IL-10 increased (P<0.05); in the CLP + PAG 12 h, 24 h group, the concentration of cTnI in serum, and pathological scores of myocardial tissue, the expression of NF-κB, the level of TNF-α increased gradually (P<0.05); and the expression of CSE mRNA and the level of IL-10 increased (P<0.05).

CONCLUSION

H2 S 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.