ArticlePloS one2017
Intracellular Ca2+ homeostasis and JAK1/STAT3 pathway are involved in the protective effect of propofol on BV2 microglia against hypoxia-induced inflammation and apoptosis.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 48 citations in OpenAlex.
- Iridoids as Multi-target Neuroprotective Agents for Ischemic Stroke: Mechanisms and Therapeutic Potential.Mini reviews in medicinal chemistry · 2026Review
- Propofol inhibits glioma growth by blocking the formation of the NF-κB/LGI4 feedback loop to activate TP53 self-transcription.Translational oncology · 2025Article
- Mechanisms of Action of Propofol in Modulating Microglial Activation in Ischemic Stroke.Molecules (Basel, Switzerland) · 2025Review
- Induction of M1 polarization in BV2 cells by propofol intervention promotes perioperative neurocognitive disorders through the NGF/CREB signaling pathway: an experimental research.International journal of surgery (London, England) · 2025Article
- Advances in research on propofol-induced postoperative cognitive dysfunction via Piezo channels.Frontiers in molecular neuroscience · 2025Review
- The Role of Intravenous Anesthetics for Neuro: Protection or Toxicity?Neuroscience bulletin · 2025Review
- Novel and emerging anesthetic drugs for the treatments of major depression: a comprehensive review of efficacy, mechanism, and outlook.Frontiers in psychiatry · 2025Review
- S-acylation of CaChronic diseases and translational medicine · 2024Review
- Research progress of propofol in alleviating cerebral ischemia/reperfusion injury.Pharmacological reports : PR · 2024Review
- Effect of General Anesthetic Agents on Microglia.Aging and disease · 2024Review
- Naringin inhibits P2X4 receptor expression on satellite glial cells in the neonatal rat dorsal root ganglion.Journal of applied biomedicine · 2023Article
- JAK2/STAT3 Signaling Pathway and Klotho Gene in Cadmium-induced Neurotoxicity In Vitro and In Vivo.Biological trace element research · 2023Article
- Microglia dynamic response and phenotype heterogeneity in neural regeneration following hypoxic-ischemic brain injury.Frontiers in immunology · 2023Review
- Neuroinflammation and status epilepticus: a narrative review unraveling a complex interplay.Frontiers in pediatrics · 2023Review
- Muscone and (+)-Borneol Cooperatively Strengthen CREB Induction of Claudin 5 in IL-1Antioxidants (Basel, Switzerland) · 2022Article
- Cobalt (II) Chloride Regulates the Invasion and Survival ofPathogens (Basel, Switzerland) · 2022Article
- The effect of propofol on hypoxia- and TNF-α-mediated BDNF/TrkB pathway dysregulation in primary rat hippocampal neurons.CNS neuroscience & therapeutics · 2022Article
- Propofol via Antioxidant Property Attenuated Hypoxia-Mediated Mitochondrial Dynamic Imbalance and Malfunction in Primary Rat Hippocampal Neurons.Oxidative medicine and cellular longevity · 2022Article
- Propofol Suppresses Microglia Inflammation by Targeting TGM2/NF-Journal of immunology research · 2021Article
- Propofol Ameliorates Microglia Activation by Targeting MicroRNA-221/222-IRF2 Axis.Journal of immunology research · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPerioperative hypoxia may induce microglial inflammation and apoptosis, resulting in brain injury. The neuroprotective effect of propofol against hypoxia has been reported, but the underlying mechanisms are far from clear. In this study, we explored whether and how propofol could attenuate microglia BV2 cells from CoCl2-induced hypoxic injury.
methodsMouse microglia BV2 cells were pretreated with propofol, and then stimulated with CoCl2. TNF-α level in the culture medium was measured by ELISA kit. Cell apoptosis and intracellular calcium concentration were measured by flow cytometry analysis. The effect of propofol on CoCl2-modulated expression of Ca2+/Calmodulin (CaM)-dependent protein kinase II (CAMKIIα), phosphorylated CAMKIIα (pCAMKIIα), STAT3, pSTAT3Y705, pSTAT3S727, ERK1/2, pERK1/2, pNFκB(p65), pro-caspase3, cleaved caspase 3, JAK1, pJAK1, JAK2, pJAK2 were detected by Western blot.
resultsIn BV2 cell, CoCl2 treatment time-dependently increased TNF-α release and induced apoptosis, which were alleviated by propofol. CoCl2 (500μmol/L, 8h) treatment increased intracellular Ca2+ level, and caused the phosphorylation of CAMKIIα, ERK1/2 and NFκB (p65), as well as the activation of caspase 3. More importantly, these effects could be modulated by 25μmol/L propofol via maintaining intracellular Ca2+ homeostasis and via up-regulating the phosphorylation of JAK1 and STAT3 at Tyr705.
conclusionPropofol could protect BV2 microglia from hypoxia-induced inflammation and apoptosis. The potential mechanisms may involve the maintaining of intracellular Ca2+ homeostasis and the activation of JAK1/STAT3 pathway.
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