Dexamethasone
(Synonyms: 地塞米松; Hexadecadrol; Prednisolone F) 目录号 : GC40775
A synthetic glucocorticoid
Cas No.:50-02-2
Sample solution is provided at 25 µL, 10mM.
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- Datasheet
| Cell experiment [1]: | |
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Cell lines |
The human choriocarcinoma cell line BeWo |
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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. |
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Reaction Conditions |
0, 20, 100, and 500 nM, 5 days |
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Applications |
Dexamethasone decreased OATP2B1 and BCRP mRNA expression and increased the MRP4 mRNA expression in a concentration-dependent manner. |
| Animal experiment [2]: | |
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Animal models |
Six to eight week-old female albino C57BL/6 mice |
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Preparation Method |
For intracranial tumor implantation, mice were injected with 1x 103 GL261 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. |
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Dosage form |
1 mg/kg/day，oral gavage |
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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. |
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References: [1]. 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. [2]. Giles AJ, et al. Dexamethasone-induced immunosuppression: mechanisms and implications for immunotherapy. J Immunother Cancer. 2018 Jun 11;6(1):51. |
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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]
地塞米松是糖皮质激素家族的一员，可以保护软骨结构和功能免受关节炎相关变化的影响，包括基质丢失、炎症和软骨活力。[1]
在离体实验中，96小时内使用10 nM至1 μM的地塞米松治疗增加了猪软骨细胞中CPPD晶体沉积。[5] 离体实验表明，在500 nM的地塞米松诱导下，GR介导了胎盘滋养层细胞中OATP2B1的下调，而法尼酸X受体介导BCRP的下调和MRP4的上调。[6] 此外，在分离的肌肉卫星细胞中给予25 nM地塞米松可使承诺性肌源祖细胞数量最大。并且，在早期分化时连续治疗0-7天10 nM地塞米松以及在5-7天时用25 nM地塞米松处理可以使成肌母细胞向肌管转化程度最高。[7]
在小鼠体内，口服每日2.5毫克/千克的治疗显著增加了表达CTLA-4的CD8 T细胞的百分比。在小鼠诱导胶原病实验中，每天静脉注射1.6毫克/千克自由地塞米松或单次注射0.4-4毫克/千克脂质体包埋地塞米松可以降低关节炎发生频率和减轻其严重程度。使用0.1毫克/千克地塞米松开始于手术后第11天，在大鼠半月板切除OA模型中降低动物对受影响爪子的疼痛反应，减少了炎症和巨噬细胞浸润，并部分挽救了关节软骨中PG损失。
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.
| Cas No. | 50-02-2 | SDF | |
| 别名 | 地塞米松; Hexadecadrol; Prednisolone F | ||
| Canonical SMILES | O=C1C=C[C@@]2(C)C(CCC3[C@]2(F)[C@@H](O)C[C@@]4(C)[C@@]3([H])C[C@@H](C)[C@]4(O)C(CO)=O)=C1 | ||
| 分子式 | C22H29FO5 | 分子量 | 392.5 |
| 溶解度 | DMSO : ≥ 56 mg/mL (142.69 mM) Ethanol : 8.33 mg/mL (21.23 mM) | 储存条件 | Store at -20°C,protect from light |
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.5478 mL | 12.7389 mL | 25.4777 mL |
| 5 mM | 0.5096 mL | 2.5478 mL | 5.0955 mL |
| 10 mM | 0.2548 mL | 1.2739 mL | 2.5478 mL |
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[Perioperative Dexamethasone]
Anaesthesist 2019 Oct;68(10):676-682.PMID:31595319DOI:10.1007/s00101-019-00672-x.
Dexamethasone is a synthetic steroid that has been used for many years in the clinical routine due to its anti-inflammatory, anti-allergic and immunosuppressive properties. Furthermore, Dexamethasone has been used for a long time for prophylaxis and treatment of chemotherapy-induced nausea and vomiting. In the meantime Dexamethasone has been approved as standard for the prophylaxis and treatment of postoperative nausea and vomiting (PONV). This review article outlines the indications and side effects of the perioperative administration of Dexamethasone.
Dexamethasone-induced immunosuppression: mechanisms and implications for immunotherapy
J Immunother Cancer 2018 Jun 11;6(1):51.PMID:29891009DOI:10.1186/s40425-018-0371-5.
Background: Corticosteroids are routinely utilized to alleviate edema in patients with intracranial lesions and are first-line agents to combat immune-related adverse events (irAEs) that arise with immune checkpoint blockade treatment. However, it is not known if or when corticosteroids can be administered without abrogating the efforts of immunotherapy. The purpose of this study was to evaluate the impact of Dexamethasone on lymphocyte activation and proliferation during checkpoint blockade to provide guidance for corticosteroid use while immunotherapy is being implemented as a cancer treatment. Methods: Lymphocyte proliferation, differentiation, and cytokine production were evaluated during Dexamethasone exposure. Human T cells were stimulated through CD3 ligation and co-stimulated either directly by CD28 ligation or by providing CD80, a shared ligand for CD28 and CTLA-4. CTLA-4 signaling was inhibited by antibody blockade using ipilimumab which has been approved for the treatment of several solid tumors. The in vivo effects of Dexamethasone during checkpoint blockade were evaluated using the GL261 syngeneic mouse intracranial model, and immune populations were profiled by flow cytometry. Results: Dexamethasone upregulated CTLA-4 mRNA and protein in CD4 and CD8 T cells and blocked CD28-mediated cell cycle entry and differentiation. Naïve T cells were most sensitive, leading to a decrease of the development of more differentiated subsets. Resistance to Dexamethasone was conferred by blocking CTLA-4 or providing strong CD28 co-stimulation prior to Dexamethasone exposure. CTLA-4 blockade increased IFNγ expression, but not IL-2, in stimulated human peripheral blood T cells exposed to Dexamethasone. Finally, we found that CTLA-4 blockade partially rescued T cell numbers in mice bearing intracranial gliomas. CTLA-4 blockade was associated with increased IFNγ-producing tumor-infiltrating T cells and extended survival of dexamethasone-treated mice. Conclusions: Dexamethasone-mediated T cell suppression diminishes naïve T cell proliferation and differentiation by attenuating the CD28 co-stimulatory pathway. However, CTLA-4, but not PD-1 blockade can partially prevent some of the inhibitory effects of Dexamethasone on the immune response.
Dexamethasone: chondroprotective corticosteroid or catabolic killer?
Eur Cell Mater 2019 Nov 22;38:246-263.PMID:31755076DOI:10.22203/eCM.v038a17.
While glucocorticoids have been used for over 50 years to treat rheumatoid and osteoarthritis pain, the prescription of glucocorticoids remains controversial because of potentially harmful side effects at the molecular, cellular and tissue levels. One member of the glucocorticoid family, Dexamethasone (DEX) has recently been demonstrated to rescue cartilage matrix loss and chondrocyte viability in animal studies and cartilage explant models of tissue injury and post-traumatic osteoarthritis, suggesting the possibility of DEX as a disease-modifying drug if used appropriately. However, the literature on the effects of DEX on cartilage reveals conflicting results on the drug's safety, depending on the dose and duration of DEX exposure as well as the model system used. Overall, DEX has been shown to protect against arthritis-related changes in cartilage structure and function, including matrix loss, inflammation and cartilage viability. These beneficial effects are not always observed in model systems using initially healthy cartilage or isolated chondrocytes, where many studies have reported significant increases in chondrocyte apoptosis. It is crucially important to understand under what conditions DEX may be beneficial or harmful to cartilage and other joint tissues and to determine potential for safe use of this glucocorticoid in the clinic as a disease-modifying drug.
Dexamethasone: Insights into Pharmacological Aspects, Therapeutic Mechanisms, and Delivery Systems
ACS Biomater Sci Eng 2022 May 9;8(5):1763-1790.PMID:35439408DOI:10.1021/acsbiomaterials.2c00026.
Dexamethasone (DEX) has been widely used to treat a variety of diseases, including autoimmune diseases, allergies, ocular disorders, cancer, and, more recently, COVID-19. However, DEX usage is often restricted in the clinic due to its poor water solubility. When administered through a systemic route, it can elicit severe side effects, such as hypertension, peptic ulcers, hyperglycemia, and hydro-electrolytic disorders. There is currently much interest in developing efficient DEX-loaded nanoformulations that ameliorate adverse disease effects inhibiting advancements in scientific research. Various nanoparticles have been developed to selectively deliver drugs without destroying healthy cells or organs in recent years. In the present review, we have summarized some of the most attractive applications of DEX-loaded delivery systems, including liposomes, polymers, hydrogels, nanofibers, silica, calcium phosphate, and hydroxyapatite. This review provides our readers with a broad spectrum of nanomedicine approaches to deliver DEX safely.
Intravenous Dexamethasone as an Analgesic: A Literature Review
AANA J 2018 Dec;86(6):488-493.PMID:31584423doi
The management of pain in surgical patients has shifted in recent years from a technique grounded in opioid administration, to a multimodal method that uses the analgesic properties of many drugs to minimize required narcotics. Multimodal analgesia has demonstrated a benefit in patient outcomes following a surgical procedure. Also of consideration is the fact that multimodal analgesia allows for less opioid to be administered to achieve acceptable pain scores, in turn reducing a patient's exposure to a potentially addicting substance. Dexamethasone is a corticosteroid that has been widely used in the perioperative setting to prevent postoperative nausea and vomiting. The analgesic properties of Dexamethasone have not been as widely acknowledged. A review of literature was conducted. Multiple studies were found that demonstrated Dexamethasone's ability to lower postoperative pain scores and reduce the amount of opioids required to achieve adequate pain scores. Single doses of Dexamethasone have demonstrated safety with minimal side effects that would be expected from corticosteroid administration. Although an elevation in blood glucose levels is seen, this is likely of little clinical significance. No difference is seen in wound healing or rates of wound infection compared with control groups.