Thioredoxin (Trx) is a hydrogen acceptor of ribonucleotide reductase and a regulator of some enzymes and receptors. It has been previously shown that significantly elevated levels of Trx expression are associated with the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs), but it is not clear how Trx regulates the effects of hydrogen peroxide (H₂O₂) on myogenic differentiation of BMSCs. Here, we report that rat BMSCs treated with a high dose (150 µm) of H₂O₂ exhibited a significant reduction in viability, cell cycling, and superoxide dismutase and glutathione peroxidase levels, and an increase in reactive oxygen species and malondialdehyde levels, which was accompanied by reductions in protein kinase B activation and forkhead Box O1, myogenic differentiation 1 and myogenin expression during myogenic differentiation. Furthermore, treatment with recombinant human Trx significantly mitigated the effects of H₂O₂ on the myogenic differentiation of BMSCs, and this was abrogated by cotreatment with wortmannin [a specific phosphatidylinositol 3‐kinase inhibitor]. In summary, our results suggest that treatment with recombinant human Trx mitigates H₂O₂‐induced oxidative stress and may promote myogenic differentiation of rat BMSCs by enhancing phosphatidylinositol 3‐kinase/protein kinase B/forkhead Box O1 signaling.

中文翻译：

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硫氧还蛋白通过增强AKT激活来减轻H2 O2对大鼠骨髓间充质干细胞成肌分化的抑制作用。

硫氧还蛋白（Trx）是核糖核苷酸还原酶的氢受体，是某些酶和受体的调节剂。以前已经表明，Trx表达的显着升高与骨髓间充质干细胞（BMSCs）的成骨分化有关，但尚不清楚Trx如何调节过氧化氢（H ₂ O ₂）对肌原性分化的影响BMSC。在这里，我们报道大鼠BMSCs用高剂量（150 µm）的H ₂ O _2治疗表现出活力，细胞周期，超氧化物歧化酶和谷胱甘肽过氧化物酶水平显着降低，活性氧和丙二醛水平升高，这伴随着蛋白激酶B激活和叉头盒O1，肌原性分化1和肌原蛋白表达的降低在成肌分化过程中。此外，重组人Trx的治疗显着减轻了H ₂ O ₂对BMSCs肌源性分化的影响，与渥曼青霉素[一种特定的磷脂酰肌醇3激酶抑制剂]共同治疗可消除这种作用。总之，我们的结果表明，重组人Trx的治疗可减轻H ₂ O ₂诱导的氧化应激，并可能通过增强磷脂酰肌醇3-激酶/蛋白激酶B /前额框O1信号传导来促进大鼠骨髓间充质干细胞的成肌分化。