Marcel Jenny1, Wolfgang Schwaiger1, David Bernhard2, Oliver A Wrulich1, Daria Cosaceanu3, Dietmar Fuchs4, Florian Ueberall1
1Division of Medical Biochemistry, Biocenter, Innsbruck Medical School, Fritz Pregl-str. 3, 6020, Innsbruck, Austria
2Division of Experimental Pathophysiology and Immunology, Biocenter, Innsbruck Medical School, Fritz Pregl-str.3, 6020, Innsbruck, Austria
3Department of Oncology-Pathology, Karolinska Institute, Cancer Centrum R 8:00, 17176, Stockholm, Sweden
4Division of Biological Chemistry, Biocenter, Innsbruck Medical School, Fritz Pregl-Str. 3, 6020, Innsbruck, Austria
DOI: 10.1186/1477-3163-4-15
ABSTRACT
The Tibetan herbal remedy PADMA 28 revealed promising results to support treatment of atherosclerosis, Charot syndrome (intermittent claudication), chronic active hepatitis and infection of the respiratory tract. The remedy was confirmed to be closely linked with anti- and pro-oxidative properties in vitro . In this study, apoptogenic and survival effects of PADMA 28 were investigated in the T cell-derived lymphocytic leukaemia cell line CEM-C7H2.
PADMA 28 led to a concentration-dependent inhibition of cell proliferation accompanied by the accumulation of CEM-C7H2 cells in subG1 phase, fragmentation of poly (ADP-ribose) polymerase (PARP) and nuclear body formation. Treatment with PADMA 28 rescued to some extent cells over-expressing Bcl-2 from apoptosis. This finding suggests that the mechanism of action of PADMA 28 may be via interference with Bcl-2 triggered survival pathways.