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ORIGINAL ARTICLE
Year : 2016  |  Volume : 12  |  Issue : 45  |  Page : 25-30

Luffa echinata Roxb. induced apoptosis in human colon cancer cell (SW-480) in the caspase-dependent manner and through a mitochondrial apoptosis pathway


1 Department of Medical Oncology, Harbin Medical University Cancer Hospital, Nangang District, Harbin, 150001, China
2 Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Nangang District, Harbin, 150001, China

Correspondence Address:
Xiao-Long Zou
Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Nangang District, Harbin, 150001
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-1296.176017

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Background: Luffa echinata Roxb. (LER) (Cucurbitaceae) showed tremendous medicinal importance and are being used for the treatment of different ailments. Objective: In this study, the antiproliferative properties and cell death mechanism induced by the extract of the fruits of LER were investigated. Materials and Methods: MTT and LDH assay were used to test the antiproliferative and cytotoxicity of LER extract, respectively. The intracellular ROS were measured by a fluorometric assay. The expression of several apoptotic-related proteins in SW-480 cells treated by LER was evaluated by Western blot analysis. Results: The methanolic extract of LER fruits inhibited the proliferation of human colon cancer cells (SW-480) in both dose- and time-dependent manners. The LER-treated cells showed obvious characteristics of cell apoptosis, including cell shrinkage, destruction of the monolayer, and condensed chromatin. In addition, treatments of various concentrations of LER extracts caused the release of lactate dehydrogenase as a dose-dependent manner via stimulation of the intracellular metabolic system. LER induced apoptosis, DNA fragmentation, and cellular ROS accumulation in SW-480 cells. Treatment of LER on SW-480 cells promoted the expression of caspases, Bax, Bad, and p53 proteins and decreased the levels of Bcl-2 and Bcl-XL. Conclusions: These results indicated that treatment with LER-induced cell death in mitochondrial apoptosis pathway by regulating pro-apoptotic proteins via the up regulation of the p53 protein. These findings highlight the potentials of LER in the treatment of human colon cancer.


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