Expression of cytokines, TNF-α and IL-1α, in MAM acetate and 1-hydroxyanthraquinone-induced colon carcinogenesis of rats

Naoki Yoshimi(Gifu University), Suzuyo Sato(Gifu University), Hiroki Makita(Gifu University), Aijin Wang(Gifu University), Yoshinobu Hirose(Gifu University), Takuji Tanaka(Gifu University), Hideki Mori(Gifu University)
Carcinogenesis
January 1, 1994
Cited by 32

Abstract

The expression of cytokines, TNF-alpha and IL-1 alpha, was examined by means of a reverse transcription followed by PCR (RT-PCR) in rat colon carcinogenesis. Forty male F344 rats were used and divided into four groups. At the start of the experiment, 20 rats were treated with methylazoxymethanol (MAM) acetate (25 mg/kg body wt, one time, i.p.) and divided into two groups; group 1 was exposed to 1% 1-hydroxyanthraquinone (1-HAQ) and group 2 was fed a basal diet during the experiment (40 weeks). Other rats were also divided into two groups; group 3 was exposed to 1% 1-HAQ as group 1, and group 4 was used as control. Tumor incidence (100%) and multiplicity (5.00 +/- 2.05) in group 1 were significantly greater than those in group 2 (20% and 0.2 +/- 0.42) and group 3 (10% and 0.10 +/- 0.32) (P < 0.01 and P < 0.01 respectively). RT-PCR technique with RNA was applied to the tissues from colon neoplasms and mucosa in each group. Expression of TNF-alpha and IL-1 alpha in the colon neoplasms was much stronger than that in the colon mucosa of each group (P < 0.001 and P < 0.01 respectively). The expression of TNF-alpha was more remarkable in the colon mucosa of group 1 than that in corresponding tissue of groups 2 and 3 (P < 0.01). The expressions of TNF-alpha and IL-1 alpha were more increased in the colon mucosa of groups 1, 2 and 3 than that in group 4 as control (P < 0.01 and P < 0.05 respectively). The results indicate that TNF-alpha and IL-1 alpha may act as growth factors in rat colon carcinogenesis by MAM acetate and 1-HAQ. In addition, the synergistic effect of 1-HAQ with MAM acetate in colon carcinogenesis might be related to biological effects of the cytokines expressed in the inflammatory condition generated by 1-HAQ.


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