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A procedure for the determination of dexketoprofen trometamol in human plasma by liquid chromatography-mass spectrometry (HPLC-MS/MS) using ibuprofen as an internal standard was proposed and validated. The matrix effect on the analyte response value was estimated; its short-term and long-term stability in a biological matrix and an aqueous acetonitrile solution was investigated. In addition, the stability of the analyte after freezing and thawing of samples was studied. It was shown that the dilution of samples by one half does not affect the accuracy and precision of the analysis. The limit of detection and the lower limit of quantification were 0.01 [micro]g/mL; the linearity range was 0.01-8.50 [micro]g/mL (R.sup.2 = 0.9974); the total analysis time was 3.5 min. Intra- and interday accuracy values were in the ranges 96.66-100.00% and 94.97-97.92%, respectively. Sample preparation, including liquid-liquid extraction with ethyl acetate in an acidic medium, is simple and fast. The developed procedure was successfully tested on real plasma samples from healthy volunteers in the framework of a comparative study of the pharmacokinetics and bioequivalence of a generic drug., Author(s): A. P. Lakeev [sup.1] [sup.2], E. A. Yanovskaya [sup.1], O. S. Bryushinina [sup.1], Yu. G. Zyuz'kova [sup.1], G. A. Frelikh [sup.1], N. Yu. Abdrashitova [sup.1], V. V. Udut [sup.1] [...]

The role of JAK/STAT3-mediated signaling pathway in the realization of the growth potential of mesenchymal precursor cells was examined in vitro. The stimulating role of JAKs and STAT3 towards proliferating activity of progenitor cells and their different role in the regulation of differentiation of the progenitor elements were demonstrated. Inhibitors of JAKs and STAT3 reduced the yield of fibroblast CFU and their mitotic activity. Blockade of JAKs accelerated and selective inactivation of STAT3 decelerated differentiation of progenitor cells. [ABSTRACT FROM AUTHOR]

Experiments of outbred rats with modeled xenobiotic load with acetylsalicylic acid (250 mg/kg for 7 days) revealed inhibition of mitochondrial respiration rate in states of rest and active phosphorylation, inhibition of succinate-dependent oxidation pathway, and a decrease in energization of organelles in the heart. For correction of the observed changes in energy production, succinic acid was preventively administered in a dose of 50 mg/kg for 7 days, which abolished the negative metabolic shifts in myocardial mitochondria. Comparison of pharmacokinetics of acetylsalicylic acid and acetylsalicylic acid against the background of succinate treatment performed on rabbits revealed complete coincidence of the studied parameters, which attests to the possibility of prevention of mitochondrial dysregulations with this Krebs cycle intermediate. [ABSTRACT FROM AUTHOR]