ArticleMolecular medicine reports2012
Mitochondria-targeted antioxidant attenuates high glucose-induced P38 MAPK pathway activation in human neuroblastoma cells.
Article in Molecular medicine reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- GLP-1 and the brain's powerhouse: a new perspective on the role of mitochondria in neuroprotection.Metabolic brain disease · 2026Review
- Mitochondria-mediated inflammation and diabetic wound healing: mechanisms and therapeutic strategies.Frontiers in pharmacology · 2026Review
- Mechanism of Glucose Water as a Neural Injection: A Perspective on Neuroinflammation.Life (Basel, Switzerland) · 2022Article
- Peptide Szeto‑Schiller 31 ameliorates doxorubicin‑induced cardiotoxicity by inhibiting the activation of the p38 MAPK signaling pathway.International journal of molecular medicine · 2021Article
- SARS-CoV-2 and mitochondrial health: implications of lifestyle and ageing.Immunity & ageing : I & A · 2020Review
- 17β‑estradiol‑induced mitochondrial dysfunction and Warburg effect in cervical cancer cells allow cell survival under metabolic stress.International journal of oncology · 2020Article
- 7,8-Dihydroxyflavone Protects High Glucose-Damaged Neuronal Cells against Oxidative Stress.Biomolecules & therapeutics · 2019Article
- Citral, A Monoterpene Protect Against High Glucose Induced Oxidative Injury in HepG2 Cell In Vitro-An Experimental Study.Journal of clinical and diagnostic research : JCDR · 2017Article
- Glucose deprivation regulates the progranulin-sortilin axis in PC12 cells.FEBS open bio · 2017Article
- Glucose promotes cell proliferation, glucose uptake and invasion in endometrial cancer cells via AMPK/mTOR/S6 and MAPK signaling.Gynecologic oncology · 2015Article
- High glucose-induced intestinal epithelial barrier damage is aggravated by syndecan-1 destruction and heparanase overexpression.Journal of cellular and molecular medicine · 2015Article
- Resveratrol protects PC12 cells from high glucose-induced neurotoxicity via PI3K/Akt/FoxO3a pathway.Cellular and molecular neurobiology · 2015Article
- Neuroprotective Effect of Radix Trichosanthis Saponins on Subarachnoid Hemorrhage.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- Antioxidant strategies in the management of diabetic neuropathy.BioMed research international · 2015Review
- Resveratrol protects DAergic PC12 cells from high glucose-induced oxidative stress and apoptosis: effect on p53 and GRP75 localization.Neurotoxicity research · 2014Article
- High glucose induces mitochondrial p53 phosphorylation by p38 MAPK in pancreatic RINm5F cells.Molecular biology reports · 2013Article
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Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive mitochondrial free radical production and the related mitogen-activated protein kinase P38 (P38 MAPK) activation are key regulators in the pathogenesis of high glucose-induced cell stress. Increasing evidence has emphasized the impact of hyperglycemia on neurons and the consequent neuronal stresses eventually resulting in neurodegeneration and neuronal death. In this study, we employed a novel mitochondria-targeted antioxidant, SS31 peptide, on high glucose-insulted neuroblastoma cells (SH-SY5Y). Our results showed that high glucose promoted significantly increased P38 phosphorylation which was efficiently suppressed by the application of the SS31 peptide under the experimental conditions. The inhibition of high glucose-induced P38 activation by the SS31 peptide was associated with the impact of the SS31 peptide on attenuating high glucose-induced mitochondrial ROS (reactive oxygen species) elevation and mitochondrial membrane potential collapse. The addition of SS31 peptide significantly attenuated high-gluose-induced apoptosis. Therefore, our study suggests that elimination of high glucose-induced mitochondrial oxidative stress helps to rescue SH-SY5Y cells from high glucose-related P38 MAPK pathway disturbances, and the SS31 peptide has the potential to serve as a new treatment strategy against hyperglycemia-instigated neuronal perturbations.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.