The cannabinoid WIN55,212-2 protects against oxidized LDL-induced inflammatory response in murine macrophages [S]
Journal of Lipid Research, ISSN: 0022-2275, Vol: 51, Issue: 8, Page: 2181-2190
2010
- 43Citations
- 58Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations43
- Citation Indexes43
- 43
- CrossRef27
- Captures58
- Readers58
- 58
Article Description
The endocannabinoid system has recently been attracted interest for its anti-inflammatory and anti-oxidative properties. In this study, we investigated the role of the endocannabinoid system in regulating the oxidized low-density lipoprotein (oxLDL)-induced inflammatory response in macrophages. RAW264.7 mouse macrophages and peritoneal macrophages isolated from Sprague-Dawley (SD) rats were exposed to oxLDL with or without the synthetic cannabinoid WIN55,212-2. To assess the inflammatory response, reactive oxygen species (ROS) and tumor necrosis factor alpha (TNF- α) levels were determined, and activation of the mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-kappa B signaling pathways were assessed. We observed that: i ) oxLDL strongly induced ROS generation and TNF- α secretion in murine macrophages; ii ) oxLDL-induced TNF- α and ROS levels could be lowered considerably by WIN55,212-2 via inhibition of MAPK (ERK1/2) signaling and NF-kappa B activity; and iii ) the effects of WIN55212-2 were attenuated by the selective CB2 receptor antagonist AM630. These results demonstrate the involvement of the endocannabinoid system in regulating the oxLDL-induced inflammatory response in macrophages, and indicate that the CB2 receptor may offer a novel pharmaceutical target for treating atherosclerosis.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0022227520370541; http://dx.doi.org/10.1194/jlr.m001511; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=77956806781&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/20305287; https://linkinghub.elsevier.com/retrieve/pii/S0022227520370541; http://www.jlr.org/lookup/doi/10.1194/jlr.M001511; https://syndication.highwire.org/content/doi/10.1194/jlr.M001511; https://dx.doi.org/10.1194/jlr.m001511
Elsevier BV
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