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Amelioration of immune cell number depletion and potentiation of depressed detoxification system of tumor-bearing mice by curcumin

Authors :
Pal, Suman
Bhattacharyya, Sankar
Choudhuri, Tathagata
Datta, Goutam K
Das, Tanya
Sa, Gaurisankar
Source :
Cancer Detection & Prevention. Sep2005, Vol. 29 Issue 5, p470-478. 9p.
Publication Year :
2005

Abstract

Abstract: Background: The true therapeutic benefit of the use of natural products, especially acceptable dietary components such as curcumin, which can spare the normal cells and boost host immunity, has opened new horizons in cancer prevention and treatment. Methods: In our model system we used Ehrlich''s ascites carcinoma cells grown in peritoneal carity of Swiss albino mice and curcumin was fed every alternative day. Results: Here, we report that curcumin administration to tumor-bearing mice decreased tumor cell number significantly in a dose-dependent manner. Furthermore, tumor-induced depletion of immune cell number of the host, as was evidenced from the decrease in bone marrow progenitor as well as thymic and splenic mononuclear cell numbers, was reintrated by curcumin. In fact, curcumin inhibited tumor-induced apoptosis of both thymocytes and splenocytes thereby restoring immune cell numbers to normal level in treated Ehrlich''s ascites carcinoma-bearing mice. Moreover, curcumin was not toxic to the host; rather in tumor-bearing mice it inhibited hematopoietic toxicity, acted as a hepatoprotective agent and activated depressed anti-oxidant and detoxification systems. Conclusion: The ability of curcumin to regress tumor as well as to protect the host from tumor-induced immunosuppression and toxicity strongly supports the candidacy of curcumin as a potential agent for the dietary therapy of cancer. [Copyright &y& Elsevier]

Details

Language :
English
ISSN :
0361090X
Volume :
29
Issue :
5
Database :
Academic Search Index
Journal :
Cancer Detection & Prevention
Publication Type :
Academic Journal
Accession number :
18744844
Full Text :
https://doi.org/10.1016/j.cdp.2005.05.003