Department of Orthopedics Ward 4, Dongzhimen Hospital Beijing University of Chinese Medicine, Beijing, 100700, China.
Department of Anesthesiology, Dongzhimen Hospital Beijing University of Chinese Medicine, Beijing, 100700, China.
In Vitro Cell Dev Biol Anim. 2023 Aug;59(7):528-535. doi: 10.1007/s11626-023-00801-2. Epub 2023 Aug 9.
Thiopental sodium (TPTS) is a barbiturate general anesthetic, while its effects on hypoxia/reoxygenation (H/R)-induced injury are still unclear. This study aimed to investigate whether TPTS exerts protective effects against the H/R-induced osteoblast cell injury and explore the underlying mechanisms. Osteoblast cell injury model was induced by the H/R condition, which was treated with or without TPTS. Cell viability and lactate dehydrogenase (LDH) release were determined by the corresponding commercial kits. The levels of oxidative stress were determined in the experimental groups. Cell apoptosis and Caspase-3 activities were determined by propidium iodide staining and substrate-based assay, respectively. Western blotting and qRT-PCR were performed to measure the mRNA and protein levels, respectively. Treatment with TPTS was able to increase cell viability and reduce LDH release in H/R-induced osteoblasts. Additionally, TPTS regulated oxidative stress in H/R-induced osteoblasts by suppressing malondialdehyde (MDA) and reactive oxygen species (ROS) as well as boosting superoxide dismutase (SOD). TPTS was able to suppress cell apoptosis by suppressing Caspase-3 activity and cleavage. TPTS exerted protective effects against cell injury and apoptosis induced by the H/R conditions, which were associated with its regulation of Akt signaling. Moreover, TPTS induced osteoblast differentiation under the H/R condition. In summary, TPTS attenuates H/R-induced injury in osteoblasts by regulating AKT signaling.
苯巴比妥钠（TPTS）是一种巴比妥类全身麻醉药，但其对缺氧/复氧（H/R）诱导损伤的作用尚不清楚。本研究旨在探讨 TPTS 是否对 H/R 诱导的成骨细胞损伤具有保护作用，并探讨其潜在机制。通过 H/R 条件诱导成骨细胞损伤模型，并用或不用 TPTS 进行处理。通过相应的商业试剂盒测定细胞活力和乳酸脱氢酶（LDH）释放。在实验组中测定氧化应激水平。通过碘化丙啶染色和基于底物的测定分别测定细胞凋亡和 Caspase-3 活性。通过 Western blot 和 qRT-PCR 分别测定 mRNA 和蛋白水平。TPTS 处理能够增加 H/R 诱导的成骨细胞中的细胞活力并降低 LDH 释放。此外，TPTS 通过抑制丙二醛（MDA）和活性氧（ROS）并提高超氧化物歧化酶（SOD）来调节 H/R 诱导的成骨细胞中的氧化应激。TPTS 能够通过抑制 Caspase-3 活性和裂解来抑制细胞凋亡。TPTS 通过调节 Akt 信号通路对 H/R 条件诱导的细胞损伤和凋亡发挥保护作用。此外，TPTS 在 H/R 条件下诱导成骨细胞分化。总之，TPTS 通过调节 AKT 信号通路减轻 H/R 诱导的成骨细胞损伤。
