| Description | Dexamethasone is a glucocorticoid receptor agonist and IL receptor modulator with anti-inflammatory, immunosuppressive, and apoptosis-inducing activities. It inhibits the production of inflammatory miRNA-155 exosomes in macrophages, significantly reduces inflammatory cytokine expression in neutrophils and monocytes, suppresses LPS-induced macrophage inflammation, and induces autophagy. It is commonly used to induce animal models of depression, muscle atrophy, and hypertension, and holds potential in COVID-19 research. |
| Targets & IC50 | CHO cells:> 20 μM, B16 F10 cells:> 20 μM, J774 cells:5.2 μM, A549 cells:> 15 μM, Macrophages:0.134 μM, B-cell:0.8 μM, HeLa S3 cells:4.1 nM, granulocyte-Macrophage cells colony stimulating factor:2.2 nM (EC50), transcription of the β2-receptor:36 nM (EC50), COS-7 cells:7.2 nM (EC50), NF-κB, IκBα, and IκBβ:0.5 nM, BV-2 cells:2.5 x 10-2 μM, Fibroblast:> 15 μM, HEK293T cells:> 20 μM, HEK293 cells:> 500 μM |
| In vitro | METHODS: Human colorectal cancer cells LoVo and HCT116 were treated with Dexamethasone (10-300 µM) for 72 h. Cell growth inhibition was detected by MTT. RESULTS: Dexamethasone dose-dependently inhibited the growth of LoVo and HCT116 cells, and the inhibition rates of 300 µM Dexamethasone were 52.6% and 58.8%, respectively. [1] METHODS: Acute lymphoblastic leukemia cells RS4;11 were treated with Dexamethasone (100 nM) for 24-36 h. Cell morphology was examined using electron microscopy. RESULTS: In cells treated with Dexamethasone for 24 h, vesicles were surrounded by double membranes, which are characteristic of autophagosomes, and contained membrane structures and/or part of the endoplasmic reticulum or a large amount of cytoplasm. In addition to the appearance of autophagosomes, the nucleus and cell morphology were initially intact, suggesting that autophagosome formation preceded cell death. Dexamethasone induces autophagy. [2] METHODS: Activated mouse and human T cells were treated with Dexamethasone (0.001-10 μM) for 48 h, and PD-1 expression was detected by Flow Cytometry. RESULTS: Dexamethasone enhanced the expression of PD-1 in mouse and human activated T cells. [3] |
| In vivo | METHODS: To investigate the anti-inflammatory effects, Dexamethasone (1-10 mg/kg) was administered as a single intraperitoneal injection to LPS-induced inflammation in C57Bl/6JBom mice. RESULTS: 10 mg/kg Dexamethasone significantly reduced neutrophils in bronchoalveolar lavage fluid.Dexamethasone treatment significantly down-regulated the levels of TNF-α, IL-1α, IL-1β, IL-6, IL-12p40 and MIP-1α mRNA. Dexamethasone exerts anti-inflammatory and antioxidant functions in acute airway inflammation. [4] METHODS: To detect anti-tumor activity in vivo, Dexamethasone (1 mg/kg) was intraperitoneally injected into SCID mice harboring the human myeloma tumor OPM2 five days per week for three weeks. RESULTS: Dexamethasone treatment significantly inhibited the growth of OPM2 tumors, indicating antitumor activity in vivo. [5] |
| Synonyms | Prednisolone F, NSC 34521, MK 125, Hexadecadrol |
| Disease Modeling Protocol | Sarcopenia model- Modeling Mechanism:
Dexamethasone induces sarcopenic pathological changes through core pathways: ① It activates the ubiquitin-proteasome system (UPS), upregulates the expression of transcription factor FoxO3α, and then promotes the expression of muscle-specific E3 ubiquitin ligases MAFbx/atrogin-1 and MuRF1, accelerating muscle protein degradation; ② It selectively damages fast-twitch muscle fibers (type II fibers), inhibits muscle protein synthesis, and leads to thinner muscle fibers and reduced muscle mass; ③ It induces muscle function decline, manifested as decreased muscle strength and reduced exercise capacity, fully mimicking the core phenotype of sarcopenic disease: "dual loss of muscle mass and muscle function". - Related Products:
Dexamethasone (T1076) - Modeling Method:
Experimental Subject: Rats: Sprague-Dawley (SD) strain, male, 6 weeks old, average body weight 180 g Dosage and Administration Route: ① Core modelling: Dexamethasone 500 μg/kg, intraperitoneal injection; ② Control treatments: Blank control group (saline intraperitoneal injection), solvent control group (distilled water oral administration); ③ Intervention validation (optional): beLP-K (1 mg/kg or 2 mg/kg), diluted in distilled water, administered orally daily Dosing Frequency and Duration Model: DEX administered once daily for 5 consecutive days. - Validation:
1. Muscle mass and morphology: - Micro-CT scans showed a significant reduction in the volume of the gastrocnemius and tibialis anterior muscles in the hind limbs of rats in the DEX group, and beLP-K intervention could inhibit the decrease in muscle mass; - After dissection and weighing, the weight of the gastrocnemius and tibialis anterior muscles in the DEX group was significantly lower than that in the control group (p<0.05), and the muscle weight recovered after beLP-K treatment; 2. Muscle function: Grip strength was significantly decreased in rats in the DEX group (p<0.001), and the grip strength improved in a dose-dependent manner after beLP-K intervention; 3. Molecular markers: Western blot analysis of rat gastrocnemius muscle tissue showed that the expression of MAFbx/atrogin-1 and MuRF1 proteins was significantly increased in the DEX group (p<0.05), and beLP-K could significantly downregulate their expression (p<0.05).
*Precautions: At the end of the experiment, the rats were euthanized by inhaling CO2. *References:Moon J,et,al. Protective Efficacy of Lactobacillus plantarum Postbiotic beLP-K in a Dexamethasone-Induced Sarcopenia Model. Int J Mol Sci. 2025 Aug 3;26(15):7504. Hypertension model- Modeling Mechanism:
Dexamethasone induces hypertension pathological changes through multiple pathways: ① It activates the NADPH oxidase pathway, promoting the generation of reactive oxygen species (ROS) and triggering oxidative stress (manifested as elevated plasma lipid peroxidation marker F₂-isoprostaglandins); ② It inhibits the expression of endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS), reducing nitric oxide (NO) production and impairing vasodilatory function; ③ It increases renal vascular resistance, affecting the regulation of renal water and sodium excretion, thereby raising blood pressure; ④ It does not depend on mitochondrial superoxide generation, and its antihypertensive mechanism is unrelated to mitochondrial ROS inhibition. - Related Products:
Dexamethasone (T1076) - Modeling Method:
Experimental Subject: Rats, Sprague-Dawley (SD), Male, Body weight 200–300 g Dosage and Administration Route: ① Core modelling: Dexamethasone, 10 μg/animal/day, subcutaneous injection; ② Control treatments: Blank control group (subcutaneous injection of 0.1 mL saline solution per animal per day), solvent control group (no additional solvent, matching injection procedure only); ③ Intervention validation (optional): Alpha-lipoic acid (antioxidant), 10 mg/animal/day, Administered orally mixed with ground feed, Commencing 4 days prior to modelling, continuing for 15 nights (covering the entire modelling period). Dosing Frequency and Duration Model: Once daily for 7 consecutive days (from experimental day 5 to day 11) - Validation:
1. Core Indicator (Blood Pressure): - Systolic blood pressure (SBP) in conscious rats was measured using a tail-cuff sphygmomanometer. After modeling, SBP increased from baseline 115±3 mmHg to 139±4 mmHg (p<0.005), significantly higher than the saline control group (119±3 mmHg); - Pretreatment with α-lipoic acid completely blocked the DEX-induced increase in SBP (SBP after modeling was 126±5 mmHg, no statistical difference), but could not reverse the established hypertension; 2. Oxidative Stress Indicators: - Plasma F₂-isoprostaglandin concentration was significantly increased (DEX group 7.1±0.6 nmol/L vs control group 4.7±0.3 nmol/L, p<0.01), and α-lipoic acid pretreatment reduced this indicator (5.7±0.2 nmol/L, p<0.05); 3. Specific Indicators: - Thymus weight was significantly reduced (DEX group 48±4.1 nmol/L). mg/100g body weight vs. control group 127±7.2 mg/100g body weight, p<0.005), verifying glucocorticoid activity; - No significant increase in renal mitochondrial superoxide (MitoSOX fluorescence detection), excluding mitochondrial ROS-mediated hypertension; 4. Auxiliary indicators: - Weight gain stagnation (DEX group body weight before and after modeling 272±9 g vs 277±7 g, no significant difference), which was significantly different from the control group (270±6 g increased to 306±7 g) (p<0.005).
*Precautions: During T11, rats were bled to death under isoflurane anesthesia between 09:00 and 11:00 AM. *References:Ong SL,et,al. The effect of alpha-lipoic acid on mitochondrial superoxide and glucocorticoid-induced hypertension. Oxid Med Cell Longev. 2013;2013:517045. |
| Animal Research | NAC was administered at three different doses (10, 100 and 500 mg/kg body weight). At the highest concentration, the acidic pH of the NAC solution was adjusted by adding NaOH. Dexamethasone was administered as a single injection of 1 or 10 mg/kg. Both drugs were dissolved in saline and 400 μl were injected intraperitoneally, either 1 h before or 1 h after LPS exposure. In one experiment, NAC (100 and 500 mg/kg) was injected successively every 4·5 h, starting 1 h before challenge (five injections in total). A control group of LPS-exposed animals were injected intraperitoneally with solvent alone (saline). Intratracheal administration was performed by instillation of 100 μl NAC (50, 100 or 500 mg/kg) or dexamethasone (10 mg/kg) into the lungs of mice anaesthetized with 15 mg/kg Rapinovet (i.v.) [4]. |