Protective Effects of Kurozu and Kurozu Moromimatsu on Dextran Sulfate Sodium-Induced Experimental Colitis

Shizuma, Toru; Ishiwata, Kazuo; Nagano, Masanobu; Mori, Hiromu; Fukuyama, Naoto

doi:10.1007/s10620-010-1432-x

Cited by 13 publications

(17 citation statements)

References 26 publications

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“…However, acetic acid, which is the main component of Kurozu, was found to be ineffective against DSS-induced colitis in our previous study (3). Further, acetic acid was not present in the Kurozu fractions used in this study.…”

contrasting

confidence: 46%

“…However, little is known about the protective effects of Kurozu against inflammatory bowel disease (IBD), such as ulcerative colitis (UC), in humans or animal models. We previously reported the protective effects of Kurozu against dextran sulfate sodium (DSS)-induced colitis in mice as a part of our study on dietary factors effective against UC (3). We found that acetic acid, which is the main component of Kurozu (3), showed no anti-colitis activity, and the active components of Kurozu remained unidentified.…”

Section: Introductionmentioning

confidence: 92%

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Therapeutic effects of four molecular-weight fractions of Kurozu against dextran sulfate sodium-induced experimental colitis

Shizuma

Nagano²,

Fujii³

et al. 2011

Turk J Gastroenterol

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contrasting

confidence: 46%

Section: Introductionmentioning

confidence: 92%

Therapeutic effects of four molecular-weight fractions of Kurozu against dextran sulfate sodium-induced experimental colitis

Shizuma

Nagano²,

Fujii³

et al. 2011

Turk J Gastroenterol

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“…We previously demonstrated the protective effects of Kurozu in a rodent model of DSS-induced colitis [18]. Oral administration of Kurozu significantly attenuated DSS-induced colitis as well as symptoms of bloody feces, body weight loss and decreased nitrotyrosine levels in the colonic epithelium, possibly by antioxidant activities.…”

Section: Anti-colitis Effects Of Kurozu (Kurosu)mentioning

confidence: 92%

“…It is manufactured by fermentation for more than a year in earthenware jars. The supernatant, known as Kurozu, contains acetic acid as well as an abundance of organic materials, minerals, and amino acids not found in other vinegars [18]. Kurozu also contains metabolites generated by lactobacillus and koji bacillus, among other microbes.…”

Section: Anti-colitis Effects Of Kurozu (Kurosu)mentioning

confidence: 99%

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Anti-Colitis Effects of Brown Rice Reported by Experimental Studies

Shizuma¹

2014

J Rice Res

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Brown (unpolished) rice is a good source of vitamins, minerals, and dietary fiber and is consumed as a health food, particularly in Asian countries. Although a limited number of studies have investigated the anti-colitis effects of brown rice, including rice bran and treated brown rice, some have reported the protective effects of brown rice in animal models of dextran sulfate sodium-induced colitis in the following settings: 1) Rice bran oil, 2) Brown rice fermented by Aspergillus oryzae, 3) Enzyme-treated rice fiber, and 4) Kurozu (fermented vinegar made from brown rice). The possible mechanisms underlying the anti-colitis effects of brown rice include anti-oxidant effects, inhibition of proinflammatory cytokine production, myeloperoxidase activity, neutrophil infiltration in the colonic mucosa, activation of nuclear factor kappa B (NF-κB), and improvement of dysbiosis. However, the active components in dietary products derived from brown rice or treated brown rice have not yet been identified. This report summarizes the studies demonstrating the anti-colitis effects of brown rice or treated brown rice in animal models of colitis.

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Cereal Vinegar Sediment Alleviates Spontaneous Ulcerative Colitis in Il‐10 Deficient Mice

Geng

Yue

Guan

et al. 2021

Molecular Nutrition Food Res

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Scope Cereal vinegar sediment (CVS) is precipitation generated during the preservation of vinegar. It has various functions such as anti‐inflammatory, anti‐tumor, hypoglycemic, and hypolipidemic. This study evaluates the effects of CVS on spontaneous colitis in Il‐10−/− mice. Methods and Results CVS (1 g kg−1 body weight) is administered to mice for 42 days. CVS alleviated epithelium damage, inhibited myeloperoxidase (MPO) activity and malondialdehyde (MDA) level, decreased gene expression of tumor necrosis factor (Tnf )‐a, inducible nitric oxide synthase (Inos), Interleukin(Il‐23) in colon tissues is found. CVS also inhibited secretion of IL‐2, IL‐6, IL‐13, Granulocyte colony stimulating factor (G‐CSF), granulocyte macrophage colony‐stimulating factor (GMCSF), Interferon (IFN)‐γ, and Regulated upon Activation, Normal T Cell Expressed and Presumably Secreted (RANTES) in serum. While CVS enhanced Regenerating Family Member 3 Gamma (Reg3γ), Mucin (Muc2, Muc3, and Muc4 gene expression, promoted intestinal epithelial cells to secrete Muc‐2, and increased the content of acetic acid in intestinal tract of Il‐10−/− mice. Additionally, CVS altered the composition of the gut microbiota by promoting the abundance of Akkermansia, Alistipes, and Lactobacillus, while inhibiting Desulfovibrio and Clostridium sensu stricto 1. These changes may be related to the regulation of steroid, fatty acids, and bile acid biosynthesis. Conclusion This study demonstrated that CVS ameliorates spontaneous ulcerative colitis in Il‐10−/− mice, which suggests CVS supplementation may serve as a protective dietary nutrient against colitis.

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Protective Effects of Kurozu and Kurozu Moromimatsu on Dextran Sulfate Sodium-Induced Experimental Colitis

Abstract: Kurozu and Kurozu-M have protective effects against DSS-induced colitis. Kurozu has anti-oxidative and anti-nitration activity.

Cited by 13 publications

References 26 publications

Therapeutic effects of four molecular-weight fractions of Kurozu against dextran sulfate sodium-induced experimental colitis

Therapeutic effects of four molecular-weight fractions of Kurozu against dextran sulfate sodium-induced experimental colitis

Anti-Colitis Effects of Brown Rice Reported by Experimental Studies

Cereal Vinegar Sediment Alleviates Spontaneous Ulcerative Colitis in Il‐10 Deficient Mice

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