3-mercaptopyruvate sulfurtransferase (3-MST) is the major source of hydrogen sulfide (H₂S) production in the brain and participates in many physiological and pathological processes. The present study was designed to investigate the role of 3-MST-derived H₂S (3-MST/H₂S) on oxygen-glucose deprivation/reoxygenation (OGD/R) injury in cerebrovascular endothelial cells (ECs). Using cerebrovascular specimens from patients with acute massive cerebral infarction (MCI), we found abnormal morphology of the endothelium and mitochondria, as well as decreases in H₂S and 3-MST levels. In an OGD/R model of ECs, 3-mercaptopyruvate (3-MP) and L-aspartic acid (L-Asp) were used to stimulate or inhibit the production of 3-MST/H₂S. The results showed that OGD/R induced significant decreases in H₂S and 3-MST levels in both ECs and mitochondria, as well as increases in oxidative stress and mitochondrial energy imbalance. Cellular oxidative stress, destruction of mitochondrial ultrastructure, accumulation of mitochondrial reactive oxygen species (ROS), reduction of mitochondrial adenosine triphosphate (ATP) synthase activity and ATP production, and decreased mitochondrial membrane potential were all significantly ameliorated by 3-MP, whereas they were exacerbated by L-Asp pretreatment. Contrary to the effects of L-Asp, the increase in RhoA activity and expression of ROCK₁ and ROCK₂ induced by OGD/R were markedly inhibited by 3-MP pretreatment in subcellular fractions without mitochondria and mitochondrial fractions. In addition, 3-MST^-/- rat ECs displayed greater oxidative stress than 3-MST^+/+ rat ECs after OGD/R injury.These findings suggest that 3-MST/H₂S protects ECs against OGD/R-induced injury, which may be related to preservation of mitochondrial function and inhibition of the RhoA/ROCK pathway.

中文翻译：

---

3-MST / H2S通过线粒体保护和RhoA / ROCK通路的抑制作用，保护脑内皮细胞免受OGD / R诱导的损伤。

3-巯基丙酮酸硫转移酶（3-MST）是大脑中产生硫化氢（H ₂ S）的主要来源，并参与许多生理和病理过程。本研究旨在研究3-MST衍生的H ₂ S（3-MST / H ₂ S）在脑血管内皮细胞（ECs）的氧-葡萄糖剥夺/复氧（OGD / R）损伤中的作用。使用来自急性大面积脑梗死（MCI）患者的脑血管标本，我们发现内皮和线粒体的形态异常，以及H ₂ S和3-MST水平降低。在EC的OGD / R模型中，使用3-巯基丙酮酸（3-MP）和L-天冬氨酸（L-Asp）刺激或抑制3-MST / H _2的产生S.结果表明，OGD / R导致EC和线粒体中H ₂ S和3-MST含量显着降低，氧化应激和线粒体能量失衡加剧。3-MP显着改善了细胞的氧化应激，线粒体超微结构的破坏，线粒体活性氧（ROS）的积累，线粒体三磷酸腺苷（ATP）合酶活性的降低和ATP的产生以及线粒体膜电位的降低，而它们分别是L-Asp预处理加剧了这种情况。与L-Asp的作用相反，RhoA活性的增加以及ROCK ₁和ROCK _2的表达在没有线粒体和线粒体组分的亚细胞组分中，通过3-MP预处理可显着抑制OGD / R诱导的TNF-α诱导。另外，OGD / R损伤后，3-MST ^-/-大鼠ECs显示出比3-MST ^{+ / +}大鼠ECs更大的氧化应激。这些发现表明3-MST / H ₂ S保护EC免受OGD / R诱导的损伤，这可能与线粒体功能的保留和RhoA / ROCK途径的抑制有关。