AI Article Synopsis
- Phospholipids in cell membranes can become oxidized (OxPL) due to oxidative stress, which is linked to the formation of atherosclerotic plaques and inflammation.
- Oxidized phospholipids like OxPAPC were found to activate pain pathways in inflamed tissues, causing increased pain sensitivity and the release of pain-related peptides.
- Treatments involving specific antibodies or peptides that target OxPAPC have shown promise in reducing pain and inflammation in preclinical models, suggesting new therapeutic avenues for inflammatory pain management.
Article Abstract
Phospholipids occurring in cell membranes and lipoproteins are converted into oxidized phospholipids (OxPL) by oxidative stress promoting atherosclerotic plaque formation. Here, OxPL were characterized as novel targets in acute and chronic inflammatory pain. Oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (OxPAPC) and its derivatives were identified in inflamed tissue by mass spectrometry and binding assays. They elicited calcium influx, hyperalgesia and induced pro-nociceptive peptide release. Genetic, pharmacological and mass spectrometric evidence in vivo as well as in vitro confirmed the role of transient receptor potential channels (TRPA1 and TRPV1) as OxPAPC targets. Treatment with the monoclonal antibody E06 or with apolipoprotein A-I mimetic peptide D-4F, capturing OxPAPC in atherosclerosis, prevented inflammatory hyperalgesia, and in vitro TRPA1 activation. Administration of D-4F or E06 to rats profoundly ameliorated mechanical hyperalgesia and inflammation in collagen-induced arthritis. These data reveal a clinically relevant role for OxPAPC in inflammation offering therapy for acute and chronic inflammatory pain treatment by scavenging OxPAPC.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5511297 | PMC |
| http://dx.doi.org/10.1038/s41598-017-05348-3 | DOI Listing |
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