Protectin D1
Protectin D1 Basic information
- Product Name:
- Protectin D1
- Synonyms:
-
- Protectin D1
- 4,7,11,13,15,19-Docosahexaenoic acid, 10,17-dihydroxy-, (4Z,7Z,10R,11E,13E,15Z,17S,19Z)-
- NPD1
- Protectin D-1,Protectin D1
- CAS:
- 660430-03-5
- MF:
- C22H32O4
- MW:
- 360.49
- Mol File:
- 660430-03-5.mol
Protectin D1 Chemical Properties
- Boiling point:
- 559.4±50.0 °C(Predicted)
- Density
- 1.048±0.06 g/cm3(Predicted)
- storage temp.
- Store at -20°C
- solubility
- DMF: 50 mg/ml; DMSO: 50 mg/ml; Ethanol: 50 mg/ml; PBS (pH 7.2): 0.1 mg/ml
- form
- Liquid
- pka
- 4.58±0.10(Predicted)
- color
- Colorless to light yellow
Protectin D1 Usage And Synthesis
Description
Protectin D1 is a specialized pro-resolving mediator (SPM) synthesized from docosahexaenoic acid (DHA; ). DHA is oxidized to 16S,17S-epoxy-protectin, which is converted to protectin D1 enzymatically. Protectin D1 increases phagocytosis of apoptotic polymorphonuclear leukocytes (PMNs) by macrophages in a non-phlogistic manner and is generated in vitro during macrophage-apoptotic interactions. It enhances phagocytosis in mice after 24 hours, but not at the initiation or peak of inflammation. It also decreases PMN infiltration in a zymosan-induced mouse model of inflammation when administered at a dose of 300 ng per animal. Protectin D1 (200 μg, i.v.) inhibits increases in neutrophil counts in bronchoalveolar fluid (BALF) and lung myeloperoxidase activity in a mouse model of pulmonary injury and inflammation induced by intratracheal LPS instillation. It also decreases pulmonary edema and promotes neutrophil apoptosis in BALF.
Uses
Protectin D1 is a potent anti-inflammatory lipid mediator.
Definition
ChEBI: Protectin D1 is a dihydroxydocosahexaenoic acid that is (4Z,7Z,11E,13E,15Z,19Z)-docosahexaenoic acid in which the two hydroxy substituents are located at positions 10 and 17 (the 10R,17S-stereoisomer). Protectin D1 is one of the specialised proresolving mediators. When produced in neural tissues, it is called neuroprotectin D1 It has a role as an anti-inflammatory agent, a neuroprotective agent, a PPARgamma agonist, an apoptosis inhibitor, a hepatoprotective agent, a human xenobiotic metabolite and a specialised pro-resolving mediator. It is a dihydroxydocosahexaenoic acid, a secondary allylic alcohol and a protectin.
in vivo
Protectin D1 (0.5, 1 μM/kg/day, i.p., once daily for 3 days) improves cardiac function and reduced infarct size in I/R-induced AMI rat model by inhibiting oxidative stress and inflammation[3]. Protectin D1 (0.08 mg/kg, i.p., single dose) exerts anti-inflammatory effects in CLP-induced sepsis rat model by reducing ROS concentration, inhibiting NALP3 inflammasome activation, and decreasing pro-inflammatory cytokine levels[4].
| Animal Model: | I/R-induced acute myocardial infarction (AMI) rat model, male Sprague Dawley rats (8 weeks old)[3] |
| Dosage: | 0.5 μM/kg, 1 μM/kg |
| Administration: | Intraperitoneal injection (i.p.), once daily for 3 days before surgery |
| Result: | Significantly reduced I/R-induced heart rate (HR), improved left ventricular ejection fraction (EF%) and fractional shortening (FS%), and reduced myocardial infarction area. |
| Animal Model: | Cecal ligation and puncture (CLP)-induced sepsis Wistar rat model (8 weeks old, 200 g)[4] |
| Dosage: | 0.08 mg/kg |
| Administration: | Intraperitoneal injection (i.p.), single dose (12 hours before surgery) |
| Result: | Significantly reduced ROS concentration in hepatocytes of CLP-induced rats, decreased NALP3, ASC, and Caspase-1 expression levels, and lowered serum IL-18 and IL-1β concentrations. |
IC 50
Human Endogenous Metabolite; IL-1β
References
[1] ANA R. RODRIGUEZ Bernd W S. Total synthesis of pro-resolving and tissue-regenerative Protectin sulfido-conjugates[J]. Tetrahedron Letters, 2015, 56 42: Pages 5811-5815. DOI: 10.1016/j.tetlet.2015.09.020
[2] JAN M. SCHWAB. Resolvin E1 and protectin D1 activate inflammation-resolution programmes[J]. Nature, 2007, 447 7146: 869-874. DOI: 10.1038/nature05877
[3] XINGWANG LI. Protectin D1 promotes resolution of inflammation in a murine model of lipopolysaccharide-induced acute lung injury via enhancing neutrophil apoptosis.[J]. Chinese Medical Journal, 2014, 127 5: 810-814.
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