Our early studies have shown that sodium thiosulfate (STS) treatment attenuated the ischemia-reperfusion (IR)-induced injury in an isolated rat heart model by decreasing apoptosis, oxidative stress, and preserving mitochondrial function. Hydrogen sulfide, the precursor molecule is reported to have similar efficacy. This study aims to investigate the role of endogenous hydrogen sulfide in STS-mediated cardioprotection against IR in an isolated rat heart model. d, l-propargylglycine (PAG), an inhibitor of cystathionine γ-lyase was used as endogenous H₂S blocker. In addition, we used the hypoxia-reoxygenation (HR) model to study the impact of STS in cardiomyocytes (H9C2) and fibroblast (3T3) cells. STS treatment to animal and cells prior to IR or HR decreased cell injury. The sensitivity of H9C2 and 3T3 cells towards HR (6 h hypoxia followed by 12 h reoxygenation) challenge varies, where, 3T3 cells exhibited higher cell death (54%). Cells treated with PAG prior to STS abrogate the protective effect in 3T3 (cell viability 61%) but not in H9C2 (cell viability 82%). Further evaluation in rat heart model showed partial recovery (46% RPP) of heart from those hearts pretreated with PAG prior to STS condition. In conclusion, we demonstrated that STS-mediated cardioprotection to IR-challenged rat heart is not fully dependent on endogenous H₂S level and this dependency may be linked to higher fibroblast content in rat heart.

中文翻译：

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硫代硫酸钠对心脏缺血-再灌注损伤的减轻部分取决于胱硫醚β合酶在心肌中的作用。

我们的早期研究表明，硫代硫酸钠（STS）处理可通过减少凋亡，氧化应激和保持线粒体功能来减轻离体大鼠心脏模型中缺血再灌注（IR）引起的损伤。据报道，前体分子硫化氢具有相似的功效。这项研究旨在调查内源性硫化氢在STS介导的离体大鼠心脏模型中对IR的心脏保护中的作用。d，使用胱硫醚γ-裂解酶抑制剂l-炔丙基甘氨酸（PAG）作为内源H _2。阻滞剂。另外，我们使用了缺氧复氧（HR）模型来研究STS对心肌细胞（H9C2）和成纤维细胞（3T3）细胞的影响。在IR或HR之前对动物和细胞进行STS处理可减少细胞损伤。H9C2和3T3细胞对HR（低氧6小时，然后再充氧12小时）攻击的敏感性各不相同，其中3T3细胞表现出更高的细胞死亡（54％）。STS之前用PAG处理的细胞在3T3（细胞活力为61％）中消除了保护作用，而在H9C2中（细胞活力为82％）则没有。在大鼠心脏模型中的进一步评估显示，在STS病情之前，使用PAG预处理的心脏部分恢复了心脏（46％RPP）。总之，我们证明了STS介导的对IR激发的大鼠心脏的心脏保护并不完全依赖于内源性H ₂S水平和这种依赖性可能与大鼠心脏中较高的成纤维细胞含量有关。