In an experimental model, a dose of 2×5 mg/kg of Dexamethasone phosphate disodium effectively curbs lipopolysaccharide (LPS)-induced inflammation. A single dose of 10 mg/kg administered intraperitoneally significantly reduces the recruitment of granulocytes and the spontaneous production of oxygen radicals in comparison to animals exposed to LPS and treated with saline alone. The treatment is significantly effective both 1 hour before and after LPS inhalation, lowering the number of granulocytes in bronchoalveolar lavage fluid (BALF) to levels comparable to those in healthy animals exposed to an aerosol of water^[3].

In studies involving rats, those treated with Dexamethasone phosphate disodium exhibited reduced food consumption and body weight compared to controls. Interestingly, these rats also weighed less than pair-fed animals despite having similar food intakes. Five days of treatment with Dexamethasone phosphate disodium led to significant increases in liver mass (by 42%) and the liver to body weight ratio (by 65%). Meanwhile, the wet weight of the gastrocnemius muscle decreased by 20% after 5 days of treatment, but this reduction was proportional to the overall body weight loss, suggesting that muscle weight loss paralleled the general reduction in body weight^[4].

Dexamethasone phosphate disodium regulates various transcription factors such as activator protein-1, nuclear factor-AT, and nuclear factor-kB. This regulation leads to the activation and repression of key genes involved in controlling the inflammatory response^[1].

Dexamethasone phosphate disodium exhibits strong inhibition of granulocyte-macrophage colony-stimulating factor (GM-CSF) release from A549 cells, demonstrating an EC50 of 2.2 nM. At a slightly higher concentration (EC50=36 nM), it induces transcription of the β2-receptor, an effect that correlates with glucocorticoid receptor (GR) DNA binding and occurs at concentrations 10-100 times higher than those needed to inhibit GM-CSF release. Furthermore, Dexamethasone phosphate disodium potently inhibits a triple combination of NF-κB, IκBα, and I-κBβ (IC50=0.5 nM), which is also linked to the inhibition of GM-CSF release^[2].