15-deoxy-Δ12,14-Prostaglandin J2 - CAS 87893-55-8
Category: Inhibitor
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Molecular Weight:
15-deoxy-Δ12,14-Prostaglandin J2 is a TRPA1 agonist and an endogenous PPARγ ligand that induces adipocyte differentiation in C3H10Y1/2 fibroblasts (EC50 = 7 μM).
≥95% by HPLC
(5Z,12E,14E)-11-Oxo-prosta-5,9,12,14-tetraen-1-oic acid
Store in a cool and dry place (or refer to the Certificate of Analysis).
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1.Beyond the classic eicosanoids: Peripherally-acting oxygenated metabolites of polyunsaturated fatty acids mediate pain associated with tissue injury and inflammation.
Shapiro H1, Singer P2, Ariel A3. Prostaglandins Leukot Essent Fatty Acids. 2016 Mar 9. pii: S0952-3278(15)30012-0. doi: 10.1016/j.plefa.2016.03.001. [Epub ahead of print]
Pain is a complex sensation that may be protective or cause undue suffering and loss of function, depending on the circumstances. Peripheral nociceptor neurons (PNs) innervate most tissues, and express ion channels, nocisensors, which depolarize the cell in response to intense stimuli and numerous substances. Inflamed tissues manifest inflammatory hyperalgesia in which the threshold for pain and the response to painful stimuli are decreased and increased, respectively. Constituents of the inflammatory milieu sensitize PNs, thereby contributing to hyperalgesia. Polyunsaturated fatty acids undergo enzymatic and free radical-mediated oxygenation into an array of bioactive metabolites, oxygenated polyunsaturated fatty acids (oxy-PUFAs), including the classic eicosanoids. Oxy-PUFA production is enhanced during inflammation. Pioneering studies by Vane and colleagues from the early 1970s first implicated classic eicosanoids in the pain associated with inflammation.
2.Nrf2 Activation Inhibits Effects of Thrombin in Human Amnion Cells and Thrombin-induced Preterm Birth in Mice.
Chigusa Y1, Hari Kishore A1, Mogami H1, Ann Word R1. J Clin Endocrinol Metab. 2016 Apr 6:jc20161059. [Epub ahead of print]
CONTEXT: Nrf2 is a key transcription factor that modulates cell defense mechanisms against endogenous and exogenous stress. Previously, we reported that thrombin increased MMPs and prostaglandin synthesis in human amnion mesenchymal cells.
3.Identification of a prostaglandin D2 metabolite as a neuritogenesis enhancer targeting the TRPV1 ion channel.
Shibata T1,2, Takahashi K1, Matsubara Y1, Inuzuka E1, Nakashima F1, Takahashi N3, Kozai D3, Mori Y3, Uchida K1. Sci Rep. 2016 Feb 16;6:21261. doi: 10.1038/srep21261.
Mast cells play important roles in allergic inflammation by secreting various mediators. In the present study, based on the finding that the medium conditioned by activated RBL-2H3 mast cells enhanced the nerve growth factor (NGF)-induced neuritogenesis of PC12 cells, we attempted to isolate an active compound from the mast cell conditioned culture medium. Our experiment identified 15-deoxy-Δ(12,14)-PGJ2 (15d-PGJ2), one of the PGD2 metabolites, as a potential enhancer of neuritogenesis. 15d-PGJ2 strongly enhanced the neuritogenesis elicited by a low-concentration of NGF that alone was insufficient to induce the neuronal differentiation. This 15d-PGJ2 effect was exerted in a Ca(2+)-dependent manner, but independently of the NGF receptor TrkA. Importantly, 15d-PGJ2 activated the transient receptor potential vanilloid-type 1 (TRPV1), a non-selective cation channel, leading to the Ca(2+) influx. In addition, we observed that (i) NGF promoted the insertion of TRPV1 into the cell surface membrane and (ii) 15d-PGJ2 covalently bound to TRPV1.
4.15d-PGJ2 Reduced Microglia Activation and Alleviated Neurological Deficit of Ischemic Reperfusion in Diabetic Rat Model.
Huang L1, Li G2, Feng X1, Wang L1. Biomed Res Int. 2015;2015:864509. doi: 10.1155/2015/864509. Epub 2015 Dec 30.
To investigate the effect of PPARγ agonist 15d-PGJ2 treatment on the microglia activation and neurological deficit of ischemia reperfusion in diabetic rat model, adult Sprague-Dawley rats were sacrificed for the research. The rats were randomly categorized into four groups: (1) sham-operated group; (2) standard ischemia group; (3) diabetic ischemia group; (4) diabetic ischemia group with diabetes and treated with 15d-PGJ2. Compared to the sham-operated group, all the ischemic groups have significantly severer neurological deficits, more TNF-α and IL-1 expression, increased labeling of apoptotic cells, increased CD68 positive staining of brain lesion, and increased volume of infarct and cerebral edema in both 24 hours and 7 days after reperfusion. Interestingly, reduced neurological deficits, decreased TNF-α and IL-1 expression, less apoptotic cells and CD68 positive staining, and alleviated infarct and cerebral edema volume were observed when 15d-PGJ2 was intraperitoneally injected after reperfusion in diabetic ischemia group, suggesting its neuroprotective role in regulating microglia activation, which may have a therapeutic application in the future.
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CAS 87893-55-8 15-deoxy-Δ12,14-Prostaglandin J2

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