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This study focused on the chemopreventive effects of Spirogyra neglecta extract (SNE) and dried S. neglecta mixed diet on the early stages of 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis in rats. Male Wistar rats were injected with DMH to initiate aberrant crypt foci (ACF) formation. In the initiation stage, SNE significantly decreased the number of ACF in the colon of DMH-treated rats. Rats that received a low dose of SNE showed enhanced activity of several detoxifying and antioxidant enzymes. In the postinitiation stage, a low dose of SNE significantly decreased the number of ACF in the colon of DMH-treated rats. It significantly reduced the number of proliferating cell nuclear antigen-positive cells and increased the number of apoptotic cells in colonic crypts. S. neglecta thus inhibited the development of the early stages of DMH-induced colon carcinogenesis in rats by modulation of xenobiotic metabolizing enzymes and inhibition of cell proliferation as well as induction of apoptosis.

Crude ethanol extracts (CEE) of purple rice was fractionated to obtain hexane soluble (HSF) and ethyl acetate soluble fractions (EASF). Total antioxidant capacity was higher in CEE than the HSF and EASF. However, HSF exhibited strong antiproliferation and apoptosis induction against colon cancer cell lines, both p53 wild-type (RKO) and mutant (SW620) strains. Then, the CEE was used to determine the effects on the progression of aberrant crypt foci (ACF), a preneoplastic lesion seen in colon carcinogenesis in rats. Male Wistar rats were subcutaneously injected of 40 mg/kg body weight dimethylhydrazin (DMH) once weekly for 2 wk. After 2 wk, rats were orally administered ethanol extract at 100 and 1000 mg/kg body weight, for 4 wk. Rats fed with only the high dose of CEE had significantly decreased numbers of ACF per rat (45.56%) and crypt multiplicity (AC/focus) (16.67%) compared to rats that received DMH alone. The result also demonstrated that CEE induced apoptosis in colonic epithelium cells of rat received colon carcinogen as detected the increasing of caspase-3 activity. This finding could be concluded that purple rice extracts inhibited aberrant colonic epithelial cell progression via apoptosis induction.

Background: Purple rice has become a natural product of interest which is widely used for health promotion. This study investigated the preventive effect of purple rice extract (PRE) mixed diet on DMH initiation of colon carcinogenesis., Materials and Methods: Rats were fed with PRE mixed diet one week before injection of DMH (40 mg/kg of body weight once a week for 2 weeks). They were killed 12 hrs after a second DMH injection to measure the level of O6-methylguanine and xenobiotic metabolizing enzyme activities., Results: In rats that received PRE, guanine methylation was reduced in the colonic mucosa, but not in the liver, whereas PRE did not affect xenobiotic conjugation, with reference to glutathione-S-transferase or UDP-glucuronyl transferase. After 5 weeks, rats that received PRE with DMH injection had fewer ACF in the colon than those treated with DMH alone. Interestingly, a PRE mixed diet inhibited the activity of bacterial β-glucuronidase in rat feces, a critical enzyme for free methylazoxymethanol (MAM) release in the rat colon. These results indicated that purple rice extract inhibited β-glucuronidase activity in the colonic lumen, causing a reduction of MAM-induced colonic mucosa DNA methylation, leaded to decelerated formation of aberrant crypt foci in the rat colon., Conclusions: The supplemented purple rice extract might thus prevent colon carcinogenesis by the alteration of the colonic environment, and thus could be further developed for neutraceutical products for colon cancer prevention.