ArticleBMC biochemistry2013
Non-steroidal anti-inflammatory drugs activate NADPH oxidase in adipocytes and raise the H2O2 pool to prevent cAMP-stimulated protein kinase a activation and inhibit lipolysis.
Article in BMC biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 27 citations in OpenAlex.
- Cellular Compartmentalization, Glutathione Transport and Its Relevance in Some Pathologies.Antioxidants (Basel, Switzerland) · 2023Review
- Niacin Status Indicators and Their Relationship with Metabolic Parameters in Dairy Cows during Early Lactation.Animals : an open access journal from MDPI · 2022Article
- Modulation of Reactive Oxygen Species Homeostasis as a Pleiotropic Effect of Commonly Used Drugs.Frontiers in aging · 2022Review
- Redox Regulation of Lipid Mobilization in Adipose Tissues.Antioxidants (Basel, Switzerland) · 2021Review
- Paracetamol (acetaminophen): A familiar drug with an unexplained mechanism of action.Temperature (Austin, Tex.) · 2021Review
- Oxidative stress resulting from the removal of endogenous catalase induces obesity by promoting hyperplasia and hypertrophy of white adipocytes.Redox biology · 2020Article
- Immunometabolism and Pulmonary Infections: Implications for Protective Immune Responses and Host-Directed Therapies.Frontiers in microbiology · 2019Review
- Differential contribution of COX-1 and COX-2 derived prostanoids to cortical spreading depression-Evoked cerebral oligemia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
- Diclofenac induces proteasome and mitochondrial dysfunction in murine cardiomyocytes and hearts.International journal of cardiology · 2016Article
- Article
- NSAIDs and Cardiovascular Diseases: Role of Reactive Oxygen Species.Oxidative medicine and cellular longevity · 2015Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNon-steroidal anti-inflammatory drugs (NSAIDs) -aspirin, naproxen, nimesulide, and piroxicam- lowered activation of type II cAMP-dependent protein kinase A (PKA-II) in isolated rat adipocytes, decreasing adrenaline- and dibutyryl cAMP (Bt2cAMP)-stimulated lipolysis. The molecular bases of insulin-like actions of NSAID were studied.
resultsBased on the reported inhibition of lipolysis by H2O2, catalase was successfully used to block NSAID inhibitory action on Bt2cAMP-stimulated lipolysis. NSAID, at (sub)micromolar range, induced an H2O2 burst in rat adipocyte plasma membranes and in whole adipocytes. NSAID-mediated rise of H2O2 was abrogated in adipocyte plasma membranes by: diphenyleneiodonium, an inhibitor of NADPH oxidase (NOX); the NOX4 antibody; and cytochrome c, trapping the NOX-formed superoxide. These three compounds prevented the inhibition of Bt2cAMP-stimulated lipolysis by NSAIDs. Inhibition of aquaporin-mediated H2O2 transport with AgNO3 in adipocytes allowed NOX activation but prevented the lipolysis inhibition promoted by NSAID: i.e., once synthesized, H2O2 must reach the lipolytic machinery. Since insulin inhibits adrenaline-stimulated lipolysis, the effect of aspirin on isoproterenol-stimulated lipolysis in rat adipocytes was studied. As expected, isoproterenol-mediated lipolysis was blunted by both insulin and aspirin.
conclusionsNSAIDs activate NOX4 in adipocytes to produce H2O2, which impairs cAMP-dependent PKA-II activation, thus preventing isoproterenol-activated lipolysis. H2O2 signaling in adipocytes is a novel and important cyclooxygenase-independent effect of NSAID.
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