P-328 Therapeutic Effects of 1-Methyl Tryptophan and Lactobacillus Spp. on AOM/DSS-Induced Institute of Cancer Research (ICR) Mouse Model

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Abstract

Background:

Colon cancer has a high record on mortality, ranking as the third common cause of death among malignant diseases. Commercially available drug, such as fluorouracil, for colorectal cancer has a low efficacy of 10% to 15% demanding an imperative need for alternative drugs. However, to do this, deeper understanding of colon carcinogenesis is necessary for therapeutic advances. Mining of anti-cancer compounds is an area of active research in the Philippines, but an observed paucity in using cancer animal models can impede the process of local drug development. This makes modelling as the main objective of this study, along with the effects of chemical and culture treatments.

Methods:

Male Institute of Cancer Research (ICR) mice were induced with the combined administration of azoxymethane and dextran sodium sulphate. Treatments include oral administrations of 1-methyl tryptophan, inhibitor of the immunosuppressive enzyme indoleamine 2,3-dioxygenase, and probiotic cultures belonging to the genus Lactobacillus, and 5-fluorouracil as positive control.

Results:

Results showed that 1-methyl tryptophan exacerbated inflammation using its surrogate markers of reduced weight, shortened colon and a slight increase of polyp count in 1-MT treated mice. For the probiotic treatment, probiotics supplemented with Lactobacillus paracasei, recovered its weight, colon length and showed a reduced polyp count as compared to 5-fluorouracil treated mice.

Conclusions:

Preliminary results using the surrogate markers reiterates that activating immune response, in the case of 1-MT, exacerbates inflammation. An observed therapeutic potential was exhibited by L. paracasei but its mechanism is yet to be elucidated. Though strain specific, some probiotics are known in affecting inflammation biomarkers, which can suggest therapeutic designs for inflammatory diseases. Inflammatory mediated carcinogenesis makes immune activation lead to a double edge-sword response by allowing cancer clearance but increases morbidity caused by inflammation. An alternative treatment is needed to balance out both responses in keeping immunity while controlling morbidity.

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