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. 2015 Sep;20(3):193-201.
doi: 10.15430/JCP.2015.20.3.193.

Chemopreventive Action of Anthocyanin-rich Black Soybean Fraction in APC (Min/+) Intestinal Polyposis Model

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Free PMC article

Chemopreventive Action of Anthocyanin-rich Black Soybean Fraction in APC (Min/+) Intestinal Polyposis Model

Mi-Young Park et al. J Cancer Prev. .
Free PMC article

Abstract

Background: Anthocyanins have been shown to inhibit cancer cell growth by suppressing oxidative stress and inflammatory responses. The purpose of this study was to investigate the effects of an anthocyanin-rich extract (AE) from black soybean coat on intestinal carcinogenesis.

Methods: Apc (Min/+) mice were fed a diet of 0.2% or 0.5% AE for 7 weeks. We analyzed the number of intestinal tumors, oxidative stress and inflammatory markers associated with β-catenin and cytosolic phospholipase A2 (cPLA2) signals. The number of intestinal tumors, and cellular expression of β-catenin were determined.

Results: The number of intestinal tumors was significantly lower in mice fed a 0.5% AE diet compared to those of the other groups. Cytosolic β-catenin expression was significantly decreased in the AE supplemented groups compared to that of the control animals. In addition, mucosa expression of cyclooxygenase-2 and cPLA2 were also significantly decreased in the 0.5% AE group, by 32% and 62%, respectively, compared to the control group.

Conclusions: These results suggest that dietary AE reduced the development of intestinal tumors, possibly through the ability to suppress oxidative stresses, decreasing inflammatory responses mediated by β-catenin associated signals.

Keywords: APCMin/+; Anthocyanins; Black soybean; Inflammation; Intestinal tumors.

Figures

Figure 1.
Figure 1.
Effect of dietary anthocyanin-rich extract (AE) on tumor formation in APCMin/+ mice. The mice were fed 0.2% or 0.5% AE supplemented diets for 7 weeks. After 7 weeks, the number of tumors was scored. Each bar represents the mean ± SE; n = 10 mice for each group. Statistical significance of the differences was evaluated by t-test (*P < 0.05). NS, not significant.
Figure 2.
Figure 2.
Effect of dietary anthocyanin-rich extract (AE) on (A) cytosolic β-catenin protein and (B) nuclear β-catenin protein level in ApcMin/+ mice. The mice were fed 0.2% or 0.5% AE supplemented diets for 7 weeks. After 7 weeks, (A) cytosolic β-catenin protein and (B) nuclear β-catenin protein level in the intestines were measured. The white bars indicate non-supplemented diets, while the black bars represents diets supplemented with AE. Each bar represents the mean ± SE; n = 10 mice for each group. The experiments are repeated 3 times. Statistical significance of differences was evaluated by t-test (**P < 0.01, ***P < 0.001). NS, not significant.
Figure 3.
Figure 3.
Effect of dietary anthocyanin-rich extract (AE) on (A) cytosolic phospholipase A2 (cPLA2) activity and (B) cPLA2 mRNA expression in ApcMin/+ mice. The mice were fed 0.2% or 0.5% AE supplemented diets for 7 weeks. After 7 weeks, (A) cPLA2 activity and (B) cPLA2 mRNA expression in the intestinal mucosa were measured. Each bar represents the mean ± SE; n = 10 mice for each group. The experiments are repeated 3 times. Statistical significance of the differences was evaluated by t-test (*P < 0.05). NS, not significant.
Figure 4.
Figure 4.
Effect of dietary anthocyanin-rich extract (AE) on (A) intestinal COX-2 and (B) serum levels of prostaglandin E2 (PGE2) in ApcMin/+ mice. The mice were fed 0.2% or 0.5% AE supplemented diets for 7 weeks. After 7 weeks, (A) intestinal COX-2 and (B) serum PGE2 level were measured. The white bars represent non-supplemented diets, and black bars indicate diets supplemented with AE. Each bar represents the mean ± SE; n = 10 mice for each group. The experiments are repeated 3 times. Statistical significance of the differences was evaluated by t-test (*P < 0.05). NS, not significant.
Figure 5.
Figure 5.
The hypothetical scheme of the mechanisms by which an anthocyanin-rich extract (AE) diet inhibits tumor formation in ApcMin/+ mice. The adenomatous polyposis coli (APC) mutation in ApcMin/+mice leads to accumulation of cytosolic and nuclear β-Cat which leads to Wnt-specific target gene translation. Reactive oxygen species (ROS) activate AA release from membrane, leading to increase of inflammatory mediators such as COX-2 and prostaglandin E2 (PGE2) which accelerate tumorigenesis. AE diet effectively inhibits cytosolic β-Cat accumulation and suppresses ROS-induced COX-2 and PGE2 expressions. β-Cat, β-catenin; AA, arachidonic acid; AXIN, Axis inhibition protein; COX-2, cyclooxygenase-2; cPLA2, cytosolic phospholipase A2; ERK, extracellular signal-regulated kinase; GSK3β, glycogen synthase kinase 3β; MAPK, mitogen-activated protein kinase; PL, phospholipid.

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