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Dexamethasone
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
Dexamethasone图片
包装与价格:
包装价格(元)
10mM (in 1mL DMSO)电议
100mg电议
500mg电议
1g电议
5g电议

产品介绍
地塞米松(Hexadecadrol)是一种糖皮质激素受体激动剂。

Cell lines

The human choriocarcinoma cell line BeWo

Preparation Method

Treated BeWo with 20, 100, and 500 nM of dexamethasone for 5 days, respectively. Cells were cultured in 96-well plates in the presence of dexamethasone at different concentrations (0, 20, 100, and 500 nM) for 5 days. MTS assay was conducted to detect the cytotoxicity of dexamethasone on BeWo cells following the manufacturer’s protocol.

Reaction Conditions

0, 20, 100, and 500 nM, 5 days

Applications

Dexamethasone decreased OATP2B1 and BCRP mRNA expression and increased the MRP4 mRNA expression in a concentration-dependent manner.

Animal models

Six to eight week-old female albino C57BL/6 mice

Preparation Method

For intracranial tumor implantation, mice were injected with 1x 103GL261 cells that were stably transduced with a firefly luciferase-mCherry lentiviral vector. Water-soluble dexamethasone was administered at 1 mg/kg/day by oral gavage.

Dosage form

1 mg/kg/day,oral gavage

Applications

Dexamethasone increased the percentage of CTLA-4-expressing CD4 T cells of tumor-bearing mice in a dose-dependent manner. CTLA-4 blockade enhances survival of dexamethasone-treated mice.

产品描述

Dexamethasone, as one member of the glucocorticoid family, can protect against arthritis-related changes in cartilage structure and function, including matrix loss, inflammation and cartilage viability.[1]

In vitro, treatment with 10 nM to 1 μM dexamethasone by 96 h increased the CPPD crystal depositionin in porcine chondrocytes.[5]In vitro experiment it indicated that GR mediates OATP2B1 downregulation induced by dexamethasone (500 nM) in placental trophoblast cells, while farnesoid X receptor mediates BCRP downregulation and MRP4 upregulation.[6]In addition, administration of 25 nM dexamethasone in isolated myogenic satellite cells results in the greatest increase in committed myogenic progenitors. And differentiation of myoblasts into myotubes was greatest with treatment of 25 nM dexamethasone at early differentiation for 5–7days and sustained treatment of 10 nM dexamethasone for 0–7 days.[7]

In vivo, treatment with 2.5 mg/kg/day orally in mice significantly increased the percent of CTLA-4-expressing CD8 T cells.[2]In vivo experiment it shown that collagen-induced mouse was daily intravenously injected of free 1.6 mg/kg Dexamethasone or a single injected of 0.4–4 mg/kg liposomalencapsulated Dexamethasone, the frequency of arthritis occurrence and lower its severity reduced.[3]With 0.1 mg/kg dexamethasone starting 11 d after surgery decrease animal pain response in the affected paw, lowers inflammation and macrophage infiltration and partially rescues PG loss in the joint cartilage in a rat meniscal transection OA model.[4]

References:
[1] Black R, et al. Dexamethasone: chondroprotective corticosteroid or catabolic killer? Eur Cell Mater. 2019 Nov 22;38:246-263.
[2] Giles AJ, et al. Dexamethasone-induced immunosuppression: mechanisms and implications for immunotherapy. J Immunother Cancer. 2018 Jun 11;6(1):51.
[3] Rauchhaus U, et al. Separating therapeutic efficacy from glucocorticoid side-effects in rodent arthritis using novel, liposomal delivery of dexamethasone phosphate: long-term suppression of arthritis facilitates interval treatment. Arthritis Res Ther. 2009;11(6):R190.
[4] Ashraf S, et al. Contributions of angiogenesis to inflammation, joint damage, and pain in a rat model of osteoarthritis. Arthritis Rheum. 2011 Sep;63(9):2700-10.
[5] Fahey M, et al. Dexamethasone promotes calcium pyrophosphate dihydrate crystal formation by articular chondrocytes. J Rheumatol. 2009 Jan;36(1):163-9.
[6] Huang W, et al. Dexamethasone induces an imbalanced fetal-placental-maternal bile acid circulation: involvement of placental transporters. BMC Med. 2021 Apr 7;19(1):87.
[7] Larson AA, et al. Effects of Dexamethasone Dose and Timing on Tissue-Engineered Skeletal Muscle Units. Cells Tissues Organs. 2018;205(4):197-207.