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BACKGROUND: The Tibetan remedy Padma 28 has been used in Europe for decades and has proved to be effective in inflammatory and atherosclerotic conditions. Beyond clinical trials, a large number of in vitro and ex vivo studies report various properties and biochemical activities of this complex herbal multicompound.OBJECTIVE: To give an overview of the complex efficacy profile of Padma 28, to review available data, to relate findings to the development of atherosclerosis and thus to discuss the antiatherogenic potential of Padma 28. METHODS: Published non-clinical original papers on Padma 28 were collected and classified according to the studied mechanisms of action. Results were correlated to the briefly described sequences of atherogenesis and various mechanisms of action were elaborated, laying particular emphasis on more recent articles. RESULTS: The complex activity profile of Padma 28 spans mainly direct and indirect anti-inflammatory proper-ties as well as further categories of biochemical actions. These can be related to the complex processes of atherogenesis. CONCLUSIONS: The described mechanisms support the therapeutic field of application of Padma 28, i.e. peripheral circulatory disorders as well as chronic inflammatory disorders. Moreover, the numerous effects as well as the diversity of sites of action allow to draw first conclusions on the conceptual design of this multicomponent formula.

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.