Intake of mulberry 1-deoxynojirimycin prevents colorectal cancer in mice

Shuang, E; Yamamoto, Kazushi; Sakamoto, Yusuke; Mizowaki, Yui; Iwagaki, Yui; Kimura, Toshiyuki; Nakagawa, Kiyotaka; Miyazawa, Teruo; Tsuduki, Tsuyoshi

doi:10.3164/jcbn.16-94

Cited by 34 publications

(5 citation statements)

References 27 publications

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“…Thus, DNJ may affect the levels of the oxidation-related molecules. DNJ can be isolated from mulberry ( Jiang et al, 2014 ; Wang et al, 2014 , 2015 ; E et al, 2017 ; Hu et al, 2017 ) or produced by Bacillus species ( Lee et al, 2013 ; Seo et al, 2013 ; Do et al, 2015 ; Cai et al, 2017 ). DNJ may be a potential drug for treating post-prandial hyperglycemia with few side effects ( Asai et al, 2011 ; Jiang et al, 2014 ).…”

Section: Introductionmentioning

confidence: 99%

1-Deoxynojirimycin (DNJ) Ameliorates Indomethacin-Induced Gastric Ulcer in Mice by Affecting NF-kappaB Signaling Pathway

Piao¹,

Sui

et al. 2018

Front. Pharmacol.

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Gastric ulcer (GU) is a main threat to public health. 1-Deoxynojirimycin (DNJ) has antioxidant and anti-inflammatory properties and may prevent GU but related mechanism remains unclear. DNJ was extracted from the supernatants of Bacillus subtilis by using ethanol and purified by using CM-Sepharose chromatography. A GU mouse model was induced by indomethacin. The functional role of DNJ in GU mice was explored by measuring the main molecules in the NF-KappaB pathway. After the model establishment, 40 GU mice were evenly assigned into five categories: IG (received vehicle control), LG (10 μg DNJ daily), MG (20 μg DNJ daily), HG (40 μg DNJ daily), and RG (0.5 mg ranitidine daily). Meanwhile, eight healthy mice were assigned as a control group (CG). After 1-month therapy, weight and gastric volume were investigated. The levels of serum inflammatory cytokines (IL-6 and TNF-α), antioxidant indices [superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH)], and oxidant biomarker malondialdehyde (MDA) were examined via ELISA. Meanwhile, inflammatory cytokine (IL-6 and TNF-α) levels, and key molecules (NF-κB p65), cyclooxygenase 1 (COX-1 and COX2) involved in NF-κB pathway, were analyzed by using Western Blot. COX-1 and COX-2 levels were further measured by immunohistochemistry. The effects of DNJ on gastric functions were explored by measuring the changes of Motilin (MOT), Substance P (SP), Somatostatin (SS), and Vasoactive intestinal peptide (VIP) in GU mouse models with ELISA Kits. The results indicated that DNJ prevented indomethacin-caused increase of gastric volume. DNJ improved histopathology of GU mice when compared with the mice from IG group (P < 0.05). DNJ consumption decreased the levels of IL-6 and TNF-α (P < 0.05). DNJ increased antioxidant indices of GU mice by improving the activities of SOD, CAT and reduced GSH, and reduced MDA levels (P < 0.05). DNJ increased the levels of prostaglandin E2, COX-1, COX2, and reduced the levels of and NF-κB p65 (P < 0.05). DNJ showed protection for gastric functions of GU mice by reducing the levels of MOT and SP, and increasing the levels of SS and VIP. DNJ treatment inactivates NF-κB signaling pathway, and increases anti-ulceration ability of the models.

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Section: Introductionmentioning

confidence: 99%

1-Deoxynojirimycin (DNJ) Ameliorates Indomethacin-Induced Gastric Ulcer in Mice by Affecting NF-kappaB Signaling Pathway

Piao¹,

Sui

et al. 2018

Front. Pharmacol.

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“…A combinatorial administration of colon carcinogen, either azoxymethane or dimethyl hydrazine (DMH) and dextran sulfate sodium (DSS) in mice was well known colon inflammatory carcinogenesis model. ( 31 ) Here, we addressed how overexpression of O -GlcNAcylation affects colon cancer development using this colon carcinogenesis model in Ogt transgenic ( Ogt -Tg) mice. ( 32 )…”

Section: Introductionmentioning

confidence: 99%

Augmented <i>O</i>-GlcNAcylation alleviates inflammation-mediated colon carcinogenesis via suppression of acute inflammation

Hiratå

Nakagawa

Moriwaki

et al. 2018

J. Clin. Biochem. Nutr.

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Colon cancer prevalence is high worldwide. O-GlcNAcylation has been associated with tumor growth in various tissues, including the colon; however, its link to carcinogenesis is not fully understood. We investigated the association of O-GlcNAcylation with colon carcinogenesis using a 1,2-dimethylhydrazine/dextran sodium sulfate-induced colon carcinogenesis model in wild type and O-GlcNAc transferase-transgenic (Ogt-Tg) mice. The incidence of colon cancer was significantly lower in Ogt-Tg than in wild type mice. The colonic length was not shortened in Ogt-Tg mice, and NF-κB p65 phosphorylation was strongly suppressed, indicating that reduction of inflammation might be related to the alleviation of colon carcinogenesis. Dextran sodium sulfate-induced acute colitis mice were used to evaluate the effect of O-GlcNAcylation on inflammation at the maximal inflammation period. In Ogt-Tg mice, NF-κB p65 phosphorylation and interleukin-1β mRNA expression were suppressed. Histochemical staining demonstrated shedding of colon epithelial cells in wild type mice a few days after dextran sodium sulfate treatment, whereas they remained essentially intact in Ogt-Tg mice. There were no significant differences on histochemical staining in the remaining epithelia between groups. These data suggest that O-GlcNAcylation could prevent colon carcinogenesis through reducing acute maximum inflammation, suggesting modulation of O-GlcNAcylation as a novel therapeutic option.

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“…Distribution of DNJ may contribute to its beneficial effects in the body and be concerned any side effects. While this study targeted the evaluation of anti-hyperglycemic effect of microorganism DNJ which exhibited in small intestine epithelium, DNJ have also been reported the targeted therapeutic effects including the improvement of lipid metabolism [ 28 ], anti-viral [ 29 ] and anti-cancer [ 30 ] activity. Moreover, it was reported the improvement of obesity through reduction of hypothalamic endoplasmic reticulum stress when intracerebroventricular administration [ 31 ], implying the effectiveness of DNJ in the body.…”

Section: Resultsmentioning

confidence: 99%

Evaluation of the anti-hyperglycemic effect and safety of microorganism 1-deoxynojirimycin

et al. 2018

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1-Deoxynojirimycin (DNJ) is a potent α-glucosidase inhibitor and thus beneficial for prevention of diabetes. While we have succeeded in obtaining the culture supernatant extract (CSE) rich in DNJ from microorganism source, information regarding its anti-hyperglycemic effect and safety were still limited. Therefore, this study was aimed to evaluate the anti-hyperglycemic effect and safety of microorganism DNJ. Oral sucrose tolerance test was performed, and the result showed that CSE was able to significantly suppress the blood glucose elevation and suggested DNJ as the main active compound. To determine its safety, the absorption and excretion of microorganism DNJ were evaluated using 15N labeling method. Our findings investigated the recovery rate of 15N from DNJ reached 80% up to 48 hours after oral administration, suggesting its rapid excretion, suggesting the safety of DNJ. This study verified the functional properties and safety of DNJ from microorganisms, suggesting its potential use for functional purpose.

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Intake of mulberry 1-deoxynojirimycin prevents colorectal cancer in mice

Cited by 34 publications

References 27 publications

1-Deoxynojirimycin (DNJ) Ameliorates Indomethacin-Induced Gastric Ulcer in Mice by Affecting NF-kappaB Signaling Pathway

1-Deoxynojirimycin (DNJ) Ameliorates Indomethacin-Induced Gastric Ulcer in Mice by Affecting NF-kappaB Signaling Pathway

Augmented <i>O</i>-GlcNAcylation alleviates inflammation-mediated colon carcinogenesis via suppression of acute inflammation

Evaluation of the anti-hyperglycemic effect and safety of microorganism 1-deoxynojirimycin

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