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- Title
Baicalin-Induced Apoptosis is Mediated by Bcl-2-Dependent, but not p53-Dependent, Pathway in Human Leukemia Cell Lines.
- Authors
Den-En Shieh; Hua-Yew Cheng; Ming-Hong Yen; Lien-Chai Chiang; Chun-Ching Lin
- Abstract
Acute lymphoblastic leukemia (ALL), especially T-acute lymphoblastic leukemia (T-ALL), is a common childhood malignant neoplastic disorder. Chemotherapy agents, particularly those that can induce apoptosis, are the major intervening strategy in the treatment of ALL. In this study, we investigated in T-ALL cell line, CCRF-CEM, the in vitro cytotoxic effect and the mechanism of action of baicalin, a compound extracted from Scutellaria baicalensis Georgi and S. rivularis Benth (Labiateae). Results demonstrated that baicalin displayed a remarkable cytotoxic effect in CCRF-CEM, with an IC50 value of 10.6 μg/ml. It triggered apoptotic effect by fragmentizing cellular DNA and arrested the cell cycle at G0/G1 phase. Baicalin (37.5 μg/ml)had not effected the expression of p53 and Fas protein. It was shown to decline the expression of Bcl-2 (22.0 pg/ml), which consequently caused the loss (52.7%)of transmembrane potential (ΔΨm) in the mitochondria after 72 hours of treatment. Baicalin (37.5 μg/ml) also elevated the amount of cytosolic cytochrome c (19.2 μg/ml), which finally triggered the activation of caspase-3 (50.1 pmol/min). In conclusion, baicalin was found to induce apoptosis in T-ALL cell lines through multiple pathways. This finding encourages further investigation of baicalin in its role as a potential candidate for chemotherapeutic agents in T-ALL.
- Subjects
APOPTOSIS; CYTOCHROME c; LYMPHOBLASTIC leukemia; CELL lines; LEUKEMIA
- Publication
American Journal of Chinese Medicine, 2006, Vol 34, Issue 2, p245
- ISSN
0192-415X
- Publication type
Article
- DOI
10.1142/S0192415X06003801