Synbiotic Combination of Djulis (Chenopodium formosanum) and Lactobacillus acidophilus Inhibits Colon Carcinogenesis in Rats

Abstract

Djulis is a functional grain containing prebiotic dietary fiber, which has an anti-cancer potential. This study examined the preventive effect of djulis alone or in combination with Lactobacillus acidophilus on colon carcinogenesis induced by 1,2-dimethylhydrazine (DMH) and dextran sulfate sodium (DSS). Rats were divided into five groups and fed B (AIN-93G, blank), C (AIN-93G, control), D (10% djulis), DLA (10% djulis plus 5 × 106 cfu L. acidophilus/g), and DHA (10% djulis plus 5 × 107 cfu L. acidophilus/g) diets, respectively. All rats except for those in group B received three doses of DMH (40 mg/kg) by intraperitoneal injection and 3% DSS in drinking water. After 10 weeks of feeding, the colon was analyzed for precancerous lesions and biomarkers. DMH and DSS treatment induced aberrant crypt foci (ACF), especially in the distal colon. D, DLA, and DHA significantly reduced the numbers of total ACF, sialomucin-producing ACF (SIM-ACF), and mucin-depleted foci (MDF) in the distal colon compared to C. Additionally, DLA and DHA further downregulated the expressions of proliferating cell nuclear antigen (PCNA) and cyclooxygenase-2 (COX-2) and regulated apoptosis-related proteins. These results suggest that synbiotic combination of djulis and L. acidophilus shows the best inhibitory effect on colon carcinogenesis via regulation of proliferative, inflammatory, and apoptotic pathways.

Dietary Supplementation of Foxtail Millet Ameliorates Colitis-Associated Colorectal Cancer in Mice via Activation of Gut Receptors and Suppression of the STAT3 Pathway

“…Western blot analyses were conducted according to previously published procedures [30]. The primary antibodies against PCNA (1:1000), p-STAT3 (1:1000), STAT3 (1:1000), and BCL2 (1:1000), and the secondary antibody goat anti-rabbit IgG-HRP (1:5000) were polyclonal antibodies purchased from Wanleibio (Shenyang, China).…”

Probiotics: A Promising Candidate for Management of Colorectal Cancer

“…Lactis BB-12, inhibited the formation of mucin depleted foci (MDF) in the middle colon and ACF-producing sialomucin (SIM-ACF), marked by increased expression of pro-apoptotic markers such as P53, caspase-3 and decreased expression of antiapoptotic Bcl-2, in 1,2dimethylhydrazine (DMH) and dextran sulfate sodium (DSS)-treated male F344 rats [104]. A decreased occurrence of ACF, SIM-ACF, and MDF was seen in DMH/DSS-treated male F344 rats when supplemented with a combination of Djulis (grain containing dietary fiber with prebiotic attributes) and Lactobacillus acidophilus LA-5, which is driven by the downregulation of proliferation and inflammation-related proteins such as PCNA and COX-2 and modulation of apoptotic pathway-related proteins such as Bcl-2, BAX, and caspase-3 [105].…”

Preventing Colorectal Cancer through Prebiotics

“…In other new researches on rats developing CRC, either genetically or by induction carcinogens such as AOM/DSS, various prebiotics such as galacto-oligosaccharides derived from lactulose [ 27 ], inulin [ 28 ], phenolic compounds such as anthocyanins and ellagic acid from Myrciaria jaboticaba ((Vell.) O.Berg) seeds [ 29 ], and Djulis ( Chenopodium formosanum ), a native cereal crop [ 30 ], had preventive effects against CRC progression ( Table 2 ). Notably, the positive impact of prebiotics on CRC progression can be seen in various human colon cell lines via the use of fructo-oligosaccharides (FOS) [ 31 ], soluble dietary fiber extracted from plantain inflorescence [ 32 ], and polysaccharide fraction from mushrooms Cantharellus cibarius [ 33 ], respectively ( Table 3 ).…”

“…Lastly, a unique mechanism of the epigenetic effects of SCFAs is the impact of butyrate on spleen tyrosine kinase (Syk), a non-receptor tyrosine kinase that plays a pivotal role in cancer progress [ 73 ]. SCFAs also inhibit COX-2 enzyme and thus decrease prostaglandin production [ 30 ]. Together, they help increase apoptotic activity and decrease the proliferation of tumour cells, while allowing normal cells to proliferate [ 9 ].…”