ArticleBMC anesthesiology2018
Mesenchymal stromal cells attenuate sevoflurane-induced apoptosis in human neuroglioma H4 cells.
Article in BMC anesthesiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Nanopathways modulating postoperative cognitive dysfunction: extracellular vesicles.Frontiers in cell and developmental biology · 2025Review
- Article
- LncRNA Riken Attenuated Sevoflurane-Induced Neuroinflammation by Regulating the MicroRNA-101a/MKP-1/JNK Pathway.Neurotoxicity research · 2022Article
- Involvement of Mitochondrial Dynamics and Mitophagy in Sevoflurane-Induced Cell Toxicity.Oxidative medicine and cellular longevity · 2021Review
- The emerging antioxidant paradigm of mesenchymal stem cell therapy.Stem cells translational medicine · 2020Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInhalation of sevoflurane can induce neuronal apoptosis, cognitive impairment and abnormal behaviors. Bone marrow mesenchymal stem cells (MSCs) can secret neurotrophic factors and cytokines to protect from oxidative stress-related neuronal apoptosis. However, whether MSCs can protect from sevoflurane-induced neuronal apoptosis and the potential mechanisms are unclear.
methodsA non-contact co-culture of MSCs with human neuroglioma H4 cells (H4 cells) was built. H4 cells were co-cultured with MSCs or without MSCs (control) for 24 h. The co-cultured H4 cells were exposed to 4% sevoflurane for 6 h. The levels of caspase-3, reactive oxygen species (ROS), adenosine triphosphate (ATP), and the release of cytochrome C were determined by Western blot and fluorescence assay.
resultsSevoflurane exposure significantly elevated the levels of cleaved caspase 3 and Bax in H4 cells. However, these phenomena were significantly offset by the co-culture with MSCs in H4 cells. Co-culture with MSCs before, but not after, sevoflurane exposure, significantly attenuated sevoflurane-induced ROS production in H4 cells. MSCs prevented sevoflurane-mediated release of cytochrome C from the mitochondria and production of ATP in H4 cells.
conclusionsOur study indicated that soluble factors secreted by MSCs attenuated the sevoflurane-induced oxidative stress and apoptosis of neuronal cells by preserving their mitochondrial function.
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