METHODS: K562 cells were treated with griseofulvin at different concentrations for 24 hours, and the inhibition effect of griseofulvin on K562 cell proliferation was assessed by tetrazolium salt colorimetric assay. Apoptosis was assessed by examining nuclear morphology and quantifying phosphatidylserine externalization, and alterations in cellular morphology were analyzed by laser scanning confocal BMS-777607 inhibitor microscopy for fluorescent analysis. Flow cytometry was used in the analysis of cell cycle, mitochondrial
membrane potential, and caspase pathways.
RESULTS: Griseofulvin could inhibit the growth of K562 cells in a dose-dependent manner with a mean (SD) inhibitory concentration of 50% value of 15.38 (1.35) mu g/mL compared with untreated controls. Apoptosis was induced in K562 cells (38.35% [2.73%] P < 0.01) by griseofulvin with the observation of both an increase in phosphatidylserine level and accumulation of chromatin nucleation in griseofulvin-treated cells. In addition, cell-cycle analysis using propidium iodide staining suggested a significant G2/M accumulation (increase from mean 17.64% [4.49%] to 48.29 [1.89%]; P < 0.01) as a result of griseofulvin
treatment. Flow cytometry analysis found that griseofulvin treatment was associated with the depolarization of the mitochondrial membrane in K562 cells. Furthermore, increased activities of caspase-3 by 22.15-fold (P < 0.01) and caspase-9 by 16.73-fold (P < 0.01) were observed in K562 cells after griseofulvin treatment compared with the untreated control; a decrease of caspase-8 activity was also Galunisertib cell line observed, but the change was not statistically significant.
CONCLUSIONS: These findings suggest that griseofulvin inhibited growth of K562 cells and induced cell apoptosis through cell-cycle arrest and selleck kinase inhibitor mitochondrial membrane potential decrease as well as caspase-3 and -9 activation. Further testing is needed to evaluate the potential of griseofulvin as a candidate in the chemotherapy of hematologic malignancies. (Curr Ther Res Clin Exp. 2010;71:384-397) (C) 2010
Elsevier HS Journals, Inc.”
“We present a seldom seen case of Takotsubo cardiomyopathy (TCM) with concurrent obstructive coronary artery disease (OCAD) and its first case surgical experience. We propose that TCM and OCAD can coexist and that the presence of OCAD should not be an exclusion criterion for the diagnosis of TCM.”
“Selectively substituted derivatives of alpha-cyclodextrin and hexa-O-tert-butyldimethylsilyl-alpha-cyclodextrin containing a definite number of acylated primary or secondary hydroxy groups were synthesized using benzoic, acetylsalicylic, and 2-(4-isobutylphenyl)propionic acid chlorides in various solvents in the presence of different bases. The acyl residues were assigned to the C(2), C(3), or C(6) atoms in the carbohydrate fragments on the basis of (13)C NMR data.