Dexmedetomidine hydrochloride (Precedex) is a potent, selective, orally active α2-adrenoceptor agonist with a Ki value of 1.08 nM. It shows 1620-fold selectivity over α1-adrenoceptors. Dexmedetomidine hydrochloride (Precedex) can protect against sepsis-induced acute lung injury through anti-inflammatory, anti-oxidative, and anti-apoptotic effects.

α2-adrenoceptor:1.08 nM (IC50)

METHODS: NR8383 alveolar macrophages were stimulated with 10 μg/ml LPS for 24 hours and then treated with Dexmedetomidine hydrochloride (Precedex) (0.01, 0.1, 1, 10, 50 μM, 2 hours) for another 2 hours. CCK-8 assay was used to evaluate the effect of different concentrations of Dexmedetomidine hydrochloride (Precedex) pretreatment on the viability of LPS-treated NR8383 cells.
RESULTS Cell viability gradually increased with increasing concentrations of Dexmedetomidine hydrochloride (Precedex). [1]

METHODS: Using C57BL/6J mice exposed to LPS, we investigated whether Dexmedetomidine hydrochloride (Precedex) (50 μg/kg, intraperitoneal injection) provides lung protection by regulating mitochondrial dynamics via the HIF-1a/HO-1 pathway in vivo.
RESULTS Dexmedetomidine hydrochloride (Precedex) alleviated lung pathological damage, reduced the oxidative stress index (OSI), improved mitochondrial dysfunction, upregulated the expression of HIF-1α and HO-1, and was accompanied by a shift in mitochondrial dynamics to fusion. [1]

In vitro HDAC assay:HDAC activity is analyzed by using an HDAC assay kit. This assay is based on the ability of DU-145 nuclear extract, which is rich in HDAC activity, to mediate the deacetylation of the biotinylated [3H]-acetyl histone H4 peptide that is bound to streptavidin agarose beads. The release of [3H]-acetate into the supernatant is measured to calculate the HDAC activity. Sodium butyrate (0.25-1 mM) is used as a positive control.