Please use this identifier to cite or link to this item: http://nopr.niscair.res.in/handle/123456789/363
Title: Activation of cell mediated immune response and apoptosis towards malignant cells with turmeric treatment in murine model
Authors: Chakravarty, Ashim K
Yasmin, Hadida
Keywords: Turmeric;Lymphocytes;Immunostimulatory;Tumor cells;Apoptotic
Issue Date: Feb-2008
Publisher: CSIR
Abstract: The effect of ethanolic turmeric extract (ETE) on murine lymphocytes vis-à-vis tumor cells was studied, in terms of its ability to activate lymphocytes and to induce apoptosis in tumor cells. Degree of activation and proliferation of lymphocytes treated with ETE was analyzed in terms of blastogenesis, DNA synthesis through ³H-thymidine incorporation and cell cycle analysis by flourescence activated cell sorter (FACS). FACS analysis was also carried out to observe the proliferation as well as apoptosis of tumor cells. Morphological condition of both the cell types in presence of ETE was examined by scanning electron microscopy (SEM). Cytotoxic capability of ETE-treated effector T lymphocytes towards tumor cells was judged in vitro by ⁵¹Cr-release assay and the growth of tumor in situ. ETE stimulated murine lymphocytes towards blastogenesis and synthesis of DNA, as revealed by increased incorporation of ³H-thymidine. FACS indicated that the lymphocytes were driven towards mitotic cycle by activating G₂-M transition. In the same count, the tumor cells mostly remained accumulated in the G₂-M phase, and thus mitotically arrested. Scanning electron photomicrographs revealed the blastoid transformation of lymphocytes and ETE-induced apoptotic condition of tumor cells. Furthermore, ETE-treated T cells were cytotoxic towards tumor cells in vitro, as shown by ⁵¹Cr- release assay. ETE administered intravenously or orally could delay the onset and growth of tumor, and thus prolonged the life span of the tumor-bearing host. The present investigation suggests potential of turmeric both to destroy the malignant cells directly and via activation of the host’s cellular immunity
Page(s): 23-29
URI: http://hdl.handle.net/123456789/363
ISSN: 0301-1208
Appears in Collections:IJBB Vol.45(1) [February 2008]

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