| First Author | Buisseret B | Year | 2019 |
| Journal | Biochim Biophys Acta Mol Cell Biol Lipids | Volume | 1864 |
| Issue | 5 | Pages | 609-618 |
| PubMed ID | 30684679 | Mgi Jnum | J:274348 |
| Mgi Id | MGI:6294825 | Doi | 10.1016/j.bbalip.2019.01.009 |
| Citation | Buisseret B, et al. (2019) Prostaglandin D2-glycerol ester decreases carrageenan-induced inflammation and hyperalgesia in mice. Biochim Biophys Acta Mol Cell Biol Lipids 1864(5):609-618 |
| abstractText | Pain is one of the cardinal signs of inflammation and is present in many inflammatory conditions. Therefore, anti-inflammatory drugs such as NSAIDs also have analgesic properties. We previously showed that prostaglandin D2-glycerol ester (PGD2-G), endogenously produced by cyclooxygenase-2 from the endocannabinoid 2-arachidonoylglycerol, has anti-inflammatory effects in vitro and in vivo that are partly mediated by DP1 receptor activation. In this work, we investigated its effect in a model of carrageenan-induced inflammatory pain. PGD2-G decreased hyperalgesia and edema, leading to a faster recovery. Moreover, PGD2-G decreased carrageenan-induced inflammatory markers in the paw as well as inflammatory cell recruitment. The effects of PGD2-G were independent from metabolite formation (PGD2 and 15d-PGJ2-G) or DP1 receptor activation in this model. Indeed PGD2 delayed recovery from hyperalgesia while 15d-PGJ2-G worsened the edema. However, while PGD2-G decreased hyperalgesia in this model of inflammatory pain, it had no effect when tested in the capsaicin-induced pain model. While the targets mediating the effects of this bioactive lipid in inflammatory pain remain to be elucidated, our findings further support the interest of anti-inflammatory lipid mediators in the management of inflammatory pain. |
