著者
Tatsuo Koyanagi Shoji Yamada
出版者
Tohoku University Medical Press
雑誌
The Tohoku Journal of Experimental Medicine (ISSN:00408727)
巻号頁・発行日
vol.94, no.1, pp.63-68, 1968 (Released:2008-11-28)
参考文献数
16
被引用文献数
1 1

The effects of supplementary feeding with niacin were investigated upon gastric acidity and vitamin B12 binding capacity of the gastric mucosa in rats which had been placed on two kinds of basal diets: low-protein diet composed of polished rice, fermented soy bean paste and cabbage, and a normal-protein diet sup-plemented with casein, gelatin and several amino acids. Five and half months after the feeding, hyperfunction of acid secreting cells associated with increased gastric acidity was observed in rats fed on the low-protein-niacin-deficient diet rather than in rats on the normal niacin-protein diet. Vitamin B12 binding capacity of the gastric mucosa of rats which has been said to be in parallel with the secretion of intrinsic factor was found to be higher in the low-protein-niacin-deficient group than in the normal-niacin-protein group.
著者
Shoji Yamada Masaki Kimura Yoshimasa Saito Hidetsugu Saito
出版者
SOCIETY FOR FREE RADICAL RESEARCH JAPAN
雑誌
Journal of Clinical Biochemistry and Nutrition (ISSN:09120009)
巻号頁・発行日
vol.63, no.2, pp.123-128, 2018 (Released:2018-09-01)
参考文献数
37
被引用文献数
2

The exact mechanisms of hepatocellular carcinoma development in non-alcoholic steatohepatitis remain unclear. In this study, we used a new class of high-fat diet, which could induce hepatocellular carcinoma development without the use of general chemical carcinogens or knockout mice. We investigated the correlation between hepatocellular carcinoma and oxidative stress/anti-oxidant effects after depletion of the gut microbiota by treatment with antibiotics. Mice fed with the steatohepatitis-inducing high-fat diet (STHD-01) for 41 weeks developed hepatocellular carcinoma. Antibiotic-treatment in mice fed with STHD-01 significantly depleted the gut microbiota and significantly ameliorated liver injury/histology. The tumor numbers of hepatocellular carcinoma were dramatically decreased by the antibiotics-treatment. We analyzed the factors involved in oxidative stress and anti-oxidant effects. Oxidative stress was elevated in mice fed with STHD-01, whereas some anti-oxidant factors were significantly elevated after antibiotics treatment. These results suggest that the gut microbiota is a key factor in improving oxidative stress induced by STHD-01 feeding.
著者
Yoshiomi Oka Shinichi Iwai Hitoshi Amano Yuko Irie Kentaro Yatomi Kakei Ryu Shoji Yamada Katsunori Inagaki Katsuji Oguchi
出版者
The Japanese Pharmacological Society
雑誌
Journal of Pharmacological Sciences (ISSN:13478613)
巻号頁・発行日
pp.1112190632, (Released:2011-12-21)
参考文献数
60
被引用文献数
82 120

Matrix metalloproteinases (MMPs) play an important role in degeneration of the matrix associated with bone and cartilage. Regulation of osteoclast activity is essential in the treatment of bone disease, including osteoporosis and rheumatoid arthritis. Polyphenols in green tea, particularly epigallocatechin-3-gallate (EGCG), inhibit MMPs expression and activity. However, the effects of the black tea polyphenol, theaflavin-3,3′-digallate (TFDG), on osteoclast and MMP activity are unknown. Therefore, we examined whether TFDG and EGCG affect MMP activity and osteoclast formation and differentiation in vitro. TFDG or EGCG (10 and 100 μM) was added to cultures of rat osteoclast precursors cells and mature osteoclasts. Numbers of multinucleated osteoclasts and actin rings decreased in polyphenol-treated cultures relative to control cultures. MMP-2 and MMP-9 activities were lower in TFDG- and EGCG-treated rat osteoclast precursor cells than in control cultures. MMP-9 mRNA levels declined significantly in TFDG-treated osteoclasts in comparison to control osteoclasts. TFDG and EGCG inhibited the formation and differentiation of osteoclasts via inhibition of MMPs. TFDG may suppress actin ring formation more effectively than EGCG. Thus, TFDG and EGCG may be suitable agents or lead compounds for the treatment of bone resorption diseases.