Thiopental sodium attenuates hypoxia/reoxygenation-induced injury in osteoblasts by modulating AKT signaling

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...

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Bibliographic Details
Published in:In vitro cellular & developmental biology. Animal 2023-08, Vol.59 (7), p.528-535
Main Authors: Hu, Chuan-yu, Li, Guo-yan, Li, Chun-Tian
Format: Article
Language:English
Subjects:
AKT protein
Animal Genetics and Genomics
Apoptosis
Biomedical and Life Sciences
Caspase-3
Cell Biology
Cell Culture
Cell injury
Cell viability
Developmental Biology
Hypoxia
Injuries
Iodides
L-Lactate dehydrogenase
Lactate dehydrogenase
Life Sciences
mRNA
Osteoblastogenesis
Osteoblasts
Oxidation
Oxidative stress
Propidium iodide
Reactive oxygen species
Sodium
Stem Cells
Substrates
Superoxide dismutase
Thiopental
Western blotting
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Summary: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.
ISSN:1071-2690
1543-706X
DOI:10.1007/s11626-023-00801-2