• Dongshi Liang, Airong Huang, Yimei Jin, Miaomiao Lin, Xiaojiao Xia, and Xiaoli Chen.
• The Second Affiliated Hospital of Wenzhou Medical University Wenzhou 325027, P. R. China.
• Am J Transl Res. 2018 Jan 1; 10 (5): 1422-1430.

AbstractThis study aimed to examine whether exogenous NaHS can protect myocardial mitochondrial injury from sepsis by enhancing the peroxisome proliferator-activated receptor gamma co-activator 1α (PGC-1α)/ nuclear factor erythroid-2-related factor 2 (NRF2) pathway and mitochondrial biosynthesis in mice. Animals were divided into sham-operated, sepsis, sepsis + 25 μmol/L NaHS, sepsis + 50 μmol/L NaHS, sepsis + 100 μmol/L NaHS, and sepsis + 200 μmol/L NaHS groups. The myocardial damage was evaluated by hematoxylin and eosin staining for myocardial microstructure and serum cardiac troponin I (cTnI) detection. The myocardial mitochondrial damage was evaluated through transmission electron microscopic observation of mitochondrial microstructure and detection of the degree of myocardial mitochondrial swelling. The adenosine triphosphate (ATP) level was used to appraise the mitochondrial function. The mRNA expression levels of Nrf2, PGC-1α, and Tfam were analyzed to explore the molecular mechanism.

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