| 包装 | 价格(元) |
| 5mg | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
Cell lines | Mouse bone-marrow-derived macrophages (BMMs) |
Preparation Method | BMMs were stimulated in complete RPMI supplemented with CSF-1 for indicated times with a combination of 20 ng/mL IL-4 , 10 μM prostaglandin E2, 100 μM 8-Br-cAMP, 20 μM Forskolin, 50 ng/mL IFN-γ, 20 ng/mL LPS, 100 μM Ap5a, 1.5 μM flurorcarbonyl cyanide phenylhydrazon, 10 nM valinomycin, 10 μM EdU, 10 μM KT5720, 10 μM H-89 or 2 μM α-amanitin under 5% CO2, atmospheric oxygen, at 37℃ in a humidified incubator. |
Reaction Conditions | 6h,10μM, 37℃ |
Applications | Prostaglandin E2 induced the expression of some genes associated with alternative—M(IL-4)—cell activation including Arg1, Il4ra, and Clec10a (CD301), prostaglandin E2 accentuated IL-4-induced expression of Arg1, IL4ra, Clec10a, CD36, and Mrc1 when both stimuli where used simultaneously (co-stimulation), although it suppressed the expression of Retnla and Pparg, prostaglandin E2 did not alter IL-4-induced phosphorylation of STAT6. Thus, prostaglandin E2 has marked STAT6-independent effects on M(IL-4) cell activation. |
Animal models | Male Wistar rats (370-430 g) |
Preparation Method | Prostaglandin E2 was dissolved in heparin/saline (50 units/ml) and infused via the aortic cannula in a cumulative manner in doses ranging from 0.01-20 ug/min. Each dose was infused for a 5 min period. |
Dosage form | 0.01ug/min-20ug/min, Prostaglandin E2 was dissolved in heparin/saline (50 units/ml) |
Applications | Dose-response curves demonstrate that under the conditions used, prostaglandin E2 produced a biphasic change in renal vascular resistance, vasodilatation started at 0.01 μg/min and was maximal at about 3 μg/min, while at the highest dose used (20μg/min) prostaglandin E2 induced renal vasoconstriction. |
| 产品描述 | Prostaglandin E2 is a major metabolite produced from arachidonic acid catalyzed by Cyclooxygenase (COX).It is also one of the most biologically active and widely studied prostaglandins. As a hormone-like substance that participate in a wide range of body functions such as the contraction and relaxation of smooth muscle, the dilation and constriction of blood vessels, control of blood pressure, and modulation of inflammation. [4] Mouse bone marrow derived naive macrophages produce prostaglandin E2 endogenously, resulting in anti-inflammatory gene expression upon differentiation induced by macrophage colony stimulating factor (M-CSF)[1]. Prostaglandin E2 has a mediator role for multiple inflammatory responses. Prostaglandin E2 receptors EP1, EP2, EP3 and EP4, are involved in the regulation of prostaglandin E2-related processes, of which[5,6], EP2 and EP4 are closely associated with inflammatio. EP2 and EP4 are involved in cytokine expression in E. coli-infected bovine endometrial tissue[7]. The affinity of PGE2 to these receptors varies according to the subtype and tissue type of the receptor, and the affinity constant (Kd) of prostaglandin E2 is about 1-10 nM. Prostaglandin E2 caused maximum relaxation of endothelin-1 precontracted vessels (EC50: 1.8×10-8M)[9].Prostaglandin E2-mediated enhancement of SPA expression in S. aureus-infected bovine endometrial tissue is dependent on EP4 receptor[4].PROSTAGLANDIN E2 induced the expression of some genes associated with alternative—M(IL-4)—cell activation including Arg1, Il4ra, and Clec10a (CD301), prostaglandin E2 accentuated IL-4-induced expression of Arg1, IL4ra, Clec10a, CD36, and Mrc1 when both stimuli where used simultaneously (co-stimulation), although it suppressed the expression of Retnla and Pparg, prostaglandin E2 did not alter IL-4-induced phosphorylation of STAT6. Thus, prostaglandin E2 has marked STAT6-independent effects on M(IL-4) cell activation[3]. The effect of intra-aortic administration of prostaglandin E2 on renal blood flow was studied in the rat anaesthetized with pentobarbitone. Dose-response curves demonstrate that under the conditions used, PROSTAGLANDIN E2 produced a biphasic change in renal vascular resistance, vasodilatation started at 0.01 μg/min and was maximal at about 3 μg/min, while at the highest dose used (20μg/min) prostaglandin E2 induced renal vasoconstriction[2].In addition, prostaglandin E2 have been shown to have complex effects on skeletal tissues, but a major effect in vivo is to increase both bone formation and bone resorption or bone remodeling, In a study in rats continuous infusion of prostaglandin E2 produced net bone loss while daily injection led to net bone gain[8]. References: |
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