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Mechanism of growth inhibitory effect of cape aloe extract in ehrlich ascites tumor cells.

Abstract
Cape aloe (Aloe ferox Miller) has been a herb well known for its cathartic properties and has also been used popularly as a health drink (juice, tea and tonic) in the United States and in Europe. Cape aloe extract also has been reported to possess several pharmacological effects, such as anti-inflammatory, anti-bacterial, anti-fungal and protective effect against liver injury. However, the investigations on an anti-tumor activity in cape aloe extract are very few and subsequent mechanisms have not been well elucidated. In this study, we examined the effect of the selective growth inhibitory activity of cape aloe extract and found that the cape aloe extract, especially the dichloromethane (CH(2)Cl(2)) extract, caused a dose-dependent growth inhibitory effect in Ehrlich ascites tumor cells (EATC), but not in mouse embryo fibroblast (NIH3T3) cells, which was used as a normal cell model. Furthermore, the CH(2)Cl(2) extract caused an accumulation of cells in the G1 phase and a decrease of cells in the S and G2/M phase of the cell cycle and inhibited DNA synthesis in a dose-dependent manner. In addition, other results suggest that cell cycle arrest and inhibition of proliferation in EATC by the CH(2)Cl(2 )extract are associated with decreased retinoblastoma protein (Rb) phosphorylation.
AuthorsSaeda Kametani, Tomoko Oikawa, Akiko Kojima-Yuasa, David Opare Kennedy, Toshio Norikura, Mayumi Honzawa, Isao Matsui-Yuasa
JournalJournal of nutritional science and vitaminology (J Nutr Sci Vitaminol (Tokyo)) Vol. 53 Issue 6 Pg. 540-6 (Dec 2007) ISSN: 0301-4800 [Print] Japan
PMID18202544 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Growth Inhibitors
  • Plant Extracts
  • Retinoblastoma Protein
  • DNA
Topics
  • Aloe
  • Animals
  • Carcinoma, Ehrlich Tumor (pathology)
  • Cell Cycle (drug effects)
  • Cell Division (drug effects)
  • Cell Line, Tumor
  • Cell Survival (drug effects)
  • DNA (biosynthesis)
  • Dose-Response Relationship, Drug
  • G1 Phase (drug effects)
  • G2 Phase (drug effects)
  • Growth Inhibitors (pharmacology)
  • Mice
  • NIH 3T3 Cells
  • Phosphorylation (drug effects)
  • Plant Extracts (pharmacology)
  • Retinoblastoma Protein (metabolism)
  • S Phase (drug effects)

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