In vitro anti-inflammatory and anticancer activities of extracts of Acalypha alopecuroidea (Euphorbiaceae).
More than 60% of conventional drugs are derived from natural compounds, some of the most effective pharmaceuticals (e.g. aspirin, quinine and various antibiotics) originate from plants or microbes, and large numbers of potentially valuable natural substances remain to be discovered. Plants with considerable medicinal potential include members of the genus Acalypha. Notably, extracts of A. platyphilla, A. fruticosa, A. siamensis, A. guatemalensis and A. wilkesiana have been recently shown to have antioxidant, antimicrobial and cytotoxic effects. In the study presented here we investigated the anti-inflammatory, anti-proliferative and pro-apoptotic activities of A. alopecuroidea, which is endemic in parts of Central America and is traditionally used by the Mopan- and Itza-Maya in the form of decoctions to treat skin conditions, and as a tea to treat stomach and urinary complaints. We demonstrate here that extracts of A. alopecuroidea can inhibit TNFalpha-induced E-selectin production, providing a mechanistic validation of its traditional use against inflammatory diseases. Furthermore, a fraction of A. alopecuroidea root extracts purified by solid phase extraction and separated by HPLC displayed strong cell cycle inhibitory activity by down-regulating and inactivating two proto-oncogenes (cyclin D1 and Cdc25A), and simultaneously inducing cyclin A, thereby disturbing orchestrated cell cycle arrest, and thus (presumably) triggering caspase 3-dependent apoptosis. The results of this study indicate that there are high prospects for purifying an active principle from A. alopecuroidea for further in vivo and preclinical studies.
Madlener
Sibylle
S
Institute of Clinical Pathology, Medical University of Vienna, A-1090 Vienna, Austria.
Svacinová
Jana
J
Kitner
Miloslav
M
Kopecky
Jirí
J
Eytner
Ruth
R
Lackner
Andreas
A
Vo
Than Phuong Nha
TP
Frisch
Richard
R
Grusch
Michael
M
De Martin
Rainer
R
Dolezal
Karel
K
Strnad
Miroslav
M
Krupitza
Georg
G
D000893:Anti-Inflammatory Agents / Q000302:isolation & purification / Q000494:pharmacology*; D000972:Antineoplastic Agents, Phytogenic / Q000302:isolation & purification / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D001943:Breast Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D053148:Caspase 3 / Q000378:metabolism; D002453:Cell Cycle / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects*; D002470:Cell Survival / Q000187:drug effects; D064447:Checkpoint Kinase 2; D042002:Chromatin Assembly and Disassembly / Q000187:drug effects; D019925:Cyclin A / Q000378:metabolism; D019938:Cyclin D1 / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D019040:E-Selectin / Q000378:metabolism; D042783:Endothelial Cells / Q000187:drug effects* / Q000276:immunology; D019665:Euphorbiaceae / Q000737:chemistry; D005260:Female; D018922:HL-60 Cells; D006801:Humans; D056626:Inflorescence; D015473:Leukemia, Promyelocytic, Acute / Q000378:metabolism* / Q000473:pathology; D009154:Mutation; D018515:Plant Leaves; D018520:Plant Shoots; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism; D013997:Time Factors; D014162:Transfection; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism; D020687:cdc25 Phosphatases / Q000378:metabolism
D000893:Anti-Inflammatory Agents; D000972:Antineoplastic Agents, Phytogenic; C530104:CCND1 protein, human; D019925:Cyclin A; D019040:E-Selectin; D014409:Tumor Necrosis Factor-alpha; D016159:Tumor Suppressor Protein p53; D019938:Cyclin D1; D064447:Checkpoint Kinase 2; C578634:CHEK2 protein, human; D017346:Protein Serine-Threonine Kinases; C517004:CDC25A protein, human; D020687:cdc25 Phosphatases; C505407:CASP3 protein, human; D053148:Caspase 3