1School of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China 2Department of Traditional Chinese Medicine, Henan Province People’s Hospital, Zhengzhou 221000, China
Abstract
Pterocephalus hookeri is a widely applied Tibetan medicinal prescription for treatment of diseases such as flu, rheumatoid arthritis, and enteritis in China. It has been reported that Pterocephalus hookeri has anti-inflammatory and analgesic actions. However, the antitumor activity of Pterocephalus hookeri remains unknown. In the present study, we demonstrate that n-butanol extracts of Pterocephalus hookeri (YSC-ZDC) has a strong antitumor activity against hepatoma carcinoma cell in vitro and in vivo. YSC-ZDC inhibited proliferation of all cancer cell lines and significantly inhibited Hep3B cells proliferation in a dose- and time-dependant manner. Transmission electron microscopy, hoechst 33258 staining, and flow cytometry analysis revealed that YSC-ZDC induced apoptosis in Hep3B cells. YSC-ZDC treatment dramatically inhibited PDK1 and Akt phosphorylation in Hep3B cells. Moreover, YSC-ZDC increased Bax expression and inhibited Bcl-2 expression. In addition, YSC-ZDC inhibited growth hepatoma xenografts in vivo with no effect on body weight and spleen index. Consistent with results in vitro, YSC-ZDC increased Bax expression and inhibited Bcl-2 expression in tumor tissue. Taken together, this study shows YSC-ZDC with an antitumor activity bothin vitro and in vivo. Its mechanism underlying is related to blocking of the Akt pathway and regulation of Bcl-2 family proteins expression.
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Apoptosis induced by the Tibetan herbal remedy PADMA 28 in the T cell-derived lymphocytic leukaemia cell line CEM-C7H2 Marcel Jenny1, Wolfgang Schwaiger1, David Bernhard2, Oliver A Wrulich1, Daria Cosaceanu3, Dietmar Fuchs4, Florian Ueberall1
1 Division of Medical Biochemistry, Biocenter, Innsbruck Medical School, Fritz Pregl-str. 3, 6020, Innsbruck, Austria 2 Division of Experimental Pathophysiology and Immunology, Biocenter, Innsbruck Medical School, Fritz Pregl-str.3, 6020, Innsbruck, Austria 3 Department of Oncology-Pathology, Karolinska Institute, Cancer Centrum R 8:00, 17176, Stockholm, Sweden 4 Division of Biological Chemistry, Biocenter, Innsbruck Medical School, Fritz Pregl-Str. 3, 6020, Innsbruck, Austria
.PADMA28 It is a mixture of a variety of different herbs (403 mg of active ingredients): Aegle marmelos (Bengal Quince) fruit (20 mg); Pimenta dioica (Allspice) fruit (25 mg); Aquilegia vulgaris (Columbine) aerial part (15 mg); Calendula officinalis (Marigold) flower (5 mg); Elettaria cardamomum (Cardamom) fruit (30 mg); Syzygium aromaticum (Clove) flower bud (12 mg); Saussurea lappa (Saussuria) root (40 mg); Hedychium spicatum (Hedychium) rhizome (10 mg); Lactuca sativa (Lettuce) leaf (6 mg); Cetraria islandica (Iceland moss) thallus (40 mg); Glycyrrhiza glabra (Licorice) root (15 mg); Azadirachta indica (Margosa) fruit (35 mg); Terminalia chebula (Myrobalan) fruit (30 mg); Plantago lanceolata (Ribwort) aerial part (15 mg); Polygonum aviculare (Knot-grass) aerial part (15 mg); Potentilla aurea (Golden Cinquefoil) aerial part (15 mg); Pterocarpus santalinus (Red Sandalwood) wood (30 mg); Sida cordifolia (Heart-leaved Sida) aerial part (10 mg); Valeriana officinalis (Valerian) root (10 mg); and Aconitum napellus (Monkshood) tuber (1 mg). Also present are 2 non-herbal components: Dextrocamphora (natural camphor) (4 mg) and Calcii sulphas pulv .(Gipsum; 20 mg).
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.
Discussion
Here we show that PADMA 28 added to T cell-derived lymphatic leukaemia cells in culture has a pronounced concentration- and time-dependent anti-proliferative effect. The inhibition of cell proliferation is accompanied by nuclear body formation a morphological signs of apoptosis. Furthermore hallmarks of apoptosis, such as the accumulation of cells in subG1 phase, and fragmentation of poly (ADP-ribose) polymerase (PARP) could be detected.
A growing body of evidence demonstrates that cell survival and cell death are largely determined by the function of Bcl-2 family members. Here we show that induction of apoptosis by PADMA 28 can be effectively counteracted by overexpression of the pro-survival protein Bcl-2. Based on our data we suggest that PADMA 28 may act in a pro-apoptotic fashion by interfering with Bcl-2 signalling.......