Description |
MJ33 is an active-site-directed, specific, competitive, and reversible phospholipase A2 (PLA2) inhibitor. MJ33 blocks the calcium-independent phospholipase A2 (iPLA2) activity of Prdx6[1]. MJ33 has a critical effect on inflammatory brain damage[2].
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Related Catalog |
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In Vitro |
MJ33, a transition-state analog competitive inhibitor of PLA2, inhibits the degradation of dipalmitoylphosphatidylcholine (DPPC) by ∼50% in both the whole lung and isolated alveolar type 2 cells. In vitro measurement of PLA2 activity in homogenate of lungs or isolated type 2 cells is markedly inhibited by MJ33 when assays at pH 4.0 in Ca2+-free medium but has no effect on Ca2+-dependent PLA2 activity at pH 8.5[3].
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In Vivo |
MJ33 (0.5 μM/kg ; by tail vein, at 24 h before MCAO) significantly blocks the increase IL-1β, IL-17 and IL-23 in rats stimulated by Prdx6 siRNA treatment[2]. Compared with the Prdx6 siRNA group, combined exposure to Prdx6 siRNA and MJ33 significantly downregulates the mRNA and protein expression of NF-κB, iNOS and COX-2[2]. Animal Model: Adult male Sprague-Dawley rats weighing 270-310 g (middle cerebral artery occlusion (MCAO) group) [2] Dosage: 0.5 μM/kg Administration: By tail vein, at 24 h before MCAO Result: Significantly blocked the increase IL-1β, IL-17 and IL-23 in rats stimulated by Prdx6 siRNA treatment.
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References |
[1]. Shanshan Y, et al. Phospholipase A2 of Peroxiredoxin 6 Plays a Critical Role in Cerebral Ischemia/Reperfusion Inflammatory Injury. Front Cell Neurosci. 2017 Apr 5;11:99. [2]. Moawad AR, et al. Deficiency of peroxiredoxin 6 or inhibition of its phospholipase A2 activity impair the in vitro sperm fertilizing competence in mice. Sci Rep. 2017 Oct 11;7(1):12994. [3]. Fisher AB, et al. Altered lung phospholipid metabolism in mice with targeted deletion of lysosomal-type phospholipase A2. J Lipid Res. 2005 Jun;46(6):1248-56.
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