ArticleOxidative medicine and cellular longevity2016
Propofol Suppressed Hypoxia/Reoxygenation-Induced Apoptosis in HBVSMC by Regulation of the Expression of Bcl-2, Bax, Caspase3, Kir6.1, and p-JNK.
Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- Crucial role of autophagy in propofol-treated neurological diseases: a comprehensive review.Frontiers in cellular neuroscience · 2023Review
- Role of ferroptosis in hypoxic preconditioning to reduce propofol neurotoxicity.Frontiers in pharmacology · 2023Article
- DHPA Protects SH-SY5Y Cells from Oxidative Stress-Induced Apoptosis via Mitochondria Apoptosis and the Keap1/Nrf2/HO-1 Signaling Pathway.Antioxidants (Basel, Switzerland) · 2022Article
- Crosstalk of the Caspase Family and Mammalian Target of Rapamycin Signaling.International journal of molecular sciences · 2021Review
- Kir Channel Molecular Physiology, Pharmacology, and Therapeutic Implications.Handbook of experimental pharmacology · 2021Review
- IFN‑γ induces apoptosis in human melanocytes by activating the JAK1/STAT1 signaling pathway.Molecular medicine reports · 2020Article
- Schizandrin A Protects Human Retinal Pigment Epithelial Cell Line ARPE-19 against HG-Induced Cell Injury by Regulation of miR-145.Molecular therapy. Nucleic acids · 2020Article
- Propofol protects human cardiac cells against chemical hypoxiainduced injury by regulating the JNK signaling pathways.Experimental and therapeutic medicine · 2020Article
- Propofol Attenuates α-Synuclein Aggregation and Neuronal Damage in a Mouse Model of Ischemic Stroke.Neuroscience bulletin · 2020Article
- Protective Effects of Adiponectin against Cobalt Chloride-Induced Apoptosis of Smooth Muscle Cells via cAMP/PKA Pathway.BioMed research international · 2020Article
- Tetrahydroxystilbene Glucoside Ameliorates Infrasound-Induced Central Nervous System (CNS) Injury by Improving Antioxidant and Anti-Inflammatory Capacity.Oxidative medicine and cellular longevity · 2020Article
- MicroRNA-20b-5p regulates propofol-preconditioning-induced inhibition of autophagy in hypoxia-and-reoxygenation-stimulated endothelial cells.Journal of biosciences · 2020Article
- Effects of Different Processed Products ofEvidence-based complementary and alternative medicine : eCAM · 2020Article
- Propofol Attenuates Hypoxia/Reoxygenation-Induced Apoptosis and Autophagy in HK-2 Cells by Inhibiting JNK Activation.Yonsei medical journal · 2019Article
- Lidocaine protects H9c2 cells from hypoxia-induced injury through regulation of the MAPK/ERK/NF-κB signaling pathway.Experimental and therapeutic medicine · 2019Article
- Propofol alleviates hypoxia-induced nerve injury in PC-12 cells by up-regulation of microRNA-153.BMC anesthesiology · 2018Article
- MicroRNA‑214 suppresses propofol‑induced neuroapoptosis through activation of phosphoinositide 3‑kinase/protein kinase B signaling by targeting phosphatase and tensin homolog expression.International journal of molecular medicine · 2018Article
- TGF-β1 Regulation of P-JNK and L-Type Calcium Channel Cav1.2 in Cortical Neurons.Journal of molecular neuroscience : MN · 2018Article
- Propofol Protects Hippocampal Neurons from Hypoxia-Reoxygenation Injury by Decreasing Calcineurin-Induced Calcium Overload and Activating YAP Signaling.Oxidative medicine and cellular longevity · 2018Article
- Epoxyeicosatrienoic Acid Inhibits the Apoptosis of Cerebral Microvascular Smooth Muscle Cells by Oxygen Glucose Deprivation via Targeting the JNK/c-Jun and mTOR Signaling Pathways.Molecules and cells · 2017Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have found that propofol may protect brain from cerebral ischemic-reperfusion injury. However, the underlying mechanism remains unclear. The effects of propofol were evaluated in HBVSMC after hypoxia/reoxygenation (H/R). Cell viability and levels of SOD, LDH, and MDA were measured. Apoptosis was detected by flow cytometry. The levels of Bax, Bcl-2, Caspase3, Sur2b, Kir6.1, JNK, p-JNK, mTOR, and p-mTOR proteins were measured by western blotting. H/R decreased cell viability and SOD activity and increased LDH leakage and MDA content in HBVSMC, all of which were significantly reversed by propofol. Propofol suppressed the levels of H/R-induced apoptosis. The expression of Bcl-2 and p-mTOR was significantly downregulated and the expression levels of Bax, Caspase3, Kir6.1, and p-JNK were upregulated following H/R injury. The ratio of p-JNK/JNK was increased; however, that of p-mTOR/mTOR decreased correspondingly. The effects on the expression of these proteins were reversed by propofol treatment. SP600125 enhanced and Everolimus attenuated the effect of propofol. These findings suggested that the protective effect of propofol against H/R injury in the HBVSMC was through the inhibition of apoptosis by inducing the expression of Bcl-2 and p-mTOR as well as inhibiting the expression levels of Bax, Caspase3, Kir6.1, and p-JNK.
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