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Chaozhou, China

Wang X.-Z.,The 188th Hospital of PLA | Wang S.-H.,The 188th Hospital of PLA | Song H.-F.,Beijing Institute of Radiation Medicine
Chinese Journal of New Drugs | Year: 2012

Objective: To investigate the pharmacokinetics of cantide, an antisense oligonucleotide, and its metabolites after multiple administration in rhesus monkeys. Methods: The pharmacokinetic behaviors of cantide and its metabolites (M1 and M2) were investigated after intravenous infusion of 8 mg ·kg-1 cantide per day for 7 days in rhesus monkeys. A dual solid phase extraction pretreatment method coupled with non-gel sieving capillary electrophoresis analysis method was used for determination of cantide and its metabolites in plasma, and their pharmacokinetic parameters were calculated. Results: After intravenous infusion of cantide to rhesus monkeys, cantide in plasma was eliminated rapidly. The first and last terminal elimination half-life (t1/2) of cantide was (57.91±23.64) min and (57.45±24.38) min, and their Cmax was (72.21±8.68) and (58.34±17.39) μg ·mL-1, respectively. The metabolites of cantide reached the Cmax immediately following cantide Cmax, and the metabolite Cmax was lower than that of the prototype. There was no statistical significant difference in plasma concentrations of cantide and its metabolites and in their pharmacokinetic parameters after multiple administration in rhesus monkeys. Conclusion: The pharmacokinetic behaviors of cantide do not change after multiple administration in rhesus monkeys, without accumulation and inducting metabolism of cantide. Source


Wang S.-H.,The 188th Hospital of PLA | Wang X.-Z.,The 188th Hospital of PLA | Dong L.-H.,Beijing Institute of Radiation Medicine | Chen F.,Beijing Institute of Radiation Medicine | Song H.-F.,Beijing Institute of Radiation Medicine
Chinese Journal of New Drugs | Year: 2013

Objective: To determine the effect of PEG-modification on the pharmacokinetics of recombinant human erythropoietin in rats. Methods: Eighteen rats were equally randomized into three groups. EPO, M-PEG-EPO and G-PEG-EPO at 5 μg·kg-1 were subcutaneously injected, respectively. Enzyme-linked immunosorbent assay (ELISA) was used to investigate the plasma concentrations of EPO, M-PEG-EPO and G-PEG-EPO. Results: After administration, the Tmax of M-PEG-EPO and G-PEG-EPO was later than that of EPO. The peak concentrations of M-PEG-EPO and G-PEG-EPO in plasma were lower than that of EPO. M-PEG-EPO and G-PEG-EPO were cleared slower as the terminal half-life was prolonged relatively. There was no statistically significant difference between M-PEG-EPO and G-PEG-EPO in pharmacokinetics parameters except AUC0~inf and Cls. Conclusion: PEG-modification of EPO can prolong the terminal half-life of EPO in rats. The pharmacokinetics of M-PEG-EPO and G-PEG-EPO in rats is similar. Source


Huang J.,The 188th Hospital of PLA | Huang J.,Shanghai University | Meng Y.,The 188th Hospital of PLA | Meng Y.,Shanghai University | And 12 more authors.
Cellular Physiology and Biochemistry | Year: 2016

Background/Aims: Human bone marrow-derived mesenchymal stem cells (hMSCs) are a promising cell source for bone engineering owing to their high potential to differentiate into osteoblasts. The bone morphogenetic protein-inducible gene homeobox a10 (HOXA10) is a critical regulator of osteogenesis. The objective of the present study was to identify microR-NAs (miRNAs) targeting HOXA10 and examine the effects on the osteogenic differentiation of hMSCs. Methods: Based on in silico analysis, HOXA10-targeting miRNAs were selected and their regulatory roles in osteoblast differentiation were investigated. Results: Six HOXA10-targeting miRNAs were identifIed by computational analysis, of which miR-320a was selected for further analysis because it was downregulated during osteogenic induction. Overexpression of miR-320a downregulated HOXA10 and significantly inhibited osteogenesis in hMSCs, as determined by the downregulation of the osteogenic markers Runx2, ALP, and OC and the inhibition of ALP activity and matrix mineralization, whereas miR-320a inhibition had the opposite effects. Furthermore, ectopic expression of HOXA10 (not including 3′-UTR) rescued the effects of miR-320a on osteogenic differentiation. Conclusion: These results suggest that miR-320a acts as a critical regulator of osteogenic differentiation of hMSCs by repressing its target HOXA10. © 2016 The Author(s) Published by S. Karger AG, Basel Source

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