Marudai Food Co.

Ōsaka, Japan

Marudai Food Co.

Ōsaka, Japan
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Sakai Y.,Oriental Yeast Co. | Kotoura S.,Marudai Food Co. | Yano T.,Oriental Yeast Co. | Yano T.,Mie University | And 5 more authors.
Bioscience, Biotechnology and Biochemistry | Year: 2011

A standard plasmid was constructed as a novel reference molecule for use in real-time quantitative PCR assays to verify the identity of beef, pork, chicken, mutton, and horseflesh. The plasmid contained a target domain of the cytochrome b (cyt b) gene and an artificial DNA sequence. Primers CO-F and CO-R, and probe CO-P were specifically designed to detect the artificial sequence. The calculated R 2 values of the standard curves (10 3-10 7 copies per reaction) for the five species ranged between 0.998 and 0.999 in the quantification analysis. The constructed plasmid provides a universal method for measuring the copy number of cyt b DNA in minced meat. This method would be a useful procedure for verifying food labels.


Mawatari S.,Institute of Rheological Function of Food | Katafuchi T.,Kyushu University | Miake K.,Marudai Food Co. | Fujino T.,Institute of Rheological Function of Food
Lipids in Health and Disease | Year: 2012

Background: Many disorders with plasmalogen deficiency have been reported. Replenishment or replacement of tissue plasmalogens of these disorders would be beneficial to the patients with these disorders, but effects of dietary plasmalogen on mammals have not been reported. Methods. Plasmalogens were purified from chicken skin. The purified plasmalogens consisted of 96.4% ethanolamine plasmalogen (PlsEtn), 2.4% choline plasmalogen (PlsCho) and 0.5% sphingomyelin (SM). A diet containing 0.1% the purified plasmalogens (PlsEtn diet) was given to rats. Relative composition of phospholipids was measured by a high performance liquid chromatography (HPLC) method that can separate intact plasmalogens and all other phospholipid classes by a single chromatographic run. Results: The PlsEtn diet given to Zucker diabetic fatty (ZDF) rats for 4 weeks caused decreases of plasma cholesterol and plasma phospholipid as compared to control diet. The other routine laboratory tests of plasma including triacylglycerol, glucose, liver and renal functions, albumin, and body weight were not different. Relative compositions of erythrocyte PlsEtn and phosphatidylethanolamine (PE) increased, and that of phosphatidylcholine (PC) decreased in PlsEtn diet group. The PlsEtn diet given to normal rats for 9 weeks again caused decrease of plasma cholesterol and phospholipid, and it induced increase of relative composition of PlsEtn of the erythrocyte membrane. The other routine laboratory tests of plasma and body weight were not different. Conclusions: Dietary PlsEtn increases relative composition of PlsEtn of erythrocyte membranes in normal and ZDF rats, and it causes decreases of plasma cholesterol and plasma phospholipids. Dietary PlsEtn for 9 weeks seemingly causes no adverse effect to health of normal rats. © 2012 Mawatari et al.; licensee BioMed Central Ltd.


Katafuchi T.,Kyushu University | Ifuku M.,Kyushu University | Mawatari S.,Institute of Rheological Function of Food | Noda M.,Kyushu University | And 3 more authors.
Annals of the New York Academy of Sciences | Year: 2012

Neuroinflammation essentially involves an activation of glial cells as the cause/effect of neurodegenerative diseases such as Alzheimer's disease (AD). Plasmalogens (Pls) are glycerophospholipids constituting cellular membranes and play significant roles in membrane fluidity and cellular processes like vesicular fusion and signal transduction. Intraperitoneal (i.p.) injection of lipopolysaccharide (LPS, 250 μg/kg) for 7 days resulted in the morphological changes and increase in number of Iba-1+ microglia showing neuroinflammation in the adult mouse hippocampus. The LPS-induced activation of glial cells was significantly attenuated by i.p. pretreatment with Pls dissolved in corn oil. In addition, systemic injection of LPS induced Aβ1-16 + neurons in the hippocampus were also abolished by application of Pls. Finally, contents of Pls in the hippocampus decreased after LPS injection, and the reduction was suppressed by administration of Pls. These findings suggest an antiamyloidogenic effect of Pls, implicating a possible therapeutic application of Pls against AD. © 2012 New York Academy of Sciences.


Yunoki K.,Obihiro University of Agriculture and Veterinary Medicine | Renaguli M.,Obihiro University of Agriculture and Veterinary Medicine | Renaguli M.,Xinjiang Agricultural University | Kinoshita M.,Obihiro University of Agriculture and Veterinary Medicine | And 6 more authors.
Journal of Agricultural and Food Chemistry | Year: 2010

Dietary sphingolipids (SL) inhibit colon carcinogenesis, reduce serum cholesterol, and improve skin barrier function and are considered to be "functional lipids". For comparative determination of the effects of SL with different chemical compositions on lipid metabolism and its related hepatic gene expression, Zucker fatty rats were fed pure sphingomyelin (SM) of animal origin and glucosylceramide (GC) of plant origin. After 45 days, the SM and GC diets led to significant reductions in hepatic lipid and plasma non-HDL cholesterol. Both SM and GC diets decreased plasma insulin levels, whereas only the GC diet increased the plasma adiponectin level. Hepatic gene expression analysis revealed increased expression of adiponectin receptor 2 (Adipor2), peroxisome proliferator-activated receptor alpha (PPARα), and pyruvate dehydrogenase kinase 4 (Pdk4). However, expression of stearoyl CoA desaturase (Scd1) was significantly decreased. These results suggest that dietary SL, even of different origins and chemical compositions, may prevent fatty liver and hypercholesterolemia through improvement of adiponectin signaling and consequent increases in insulin sensitivity. © 2010 American Chemical Society.


Hossain Md.S.,Kyushu University | Ifuku M.,Kyushu University | Take S.,Kyushu University | Kawamura J.,Marudai Food Co. | And 2 more authors.
PLoS ONE | Year: 2013

Neuronal cells are susceptible to many stresses, which will cause the apoptosis and neurodegenerative diseases. The precise molecular mechanism behind the neuronal protection against these apoptotic stimuli is necessary for drug discovery. In the present study, we have found that plasmalogens (Pls), which are glycerophospholipids containing vinyl ether linkage at sn-1 position, can protect the neuronal cell death upon serum deprivation. Interestingly, caspse-9, but not caspase-8 and caspase-12, was cleaved upon the serum starvation in Neuro-2A cells. Pls treatments effectively reduced the activation of caspase-9. Furthermore, cellular signaling experiments showed that Pls enhanced phosphorylation of the phosphoinositide 3-kinase (PI3K)-dependent serine/threoninespecific protein kinase AKT and extracellular-signal-regulated kinases ERK1/2. PI3K/AKT inhibitor LY294002 and MAPK/ERK kinase (MEK) inhibitor U0126 treatments study clearly indicated that Pls-mediated cell survival was dependent on the activation of these kinases. In addition, Pls also inhibited primary mouse hippocampal neuronal cell death induced by nutrient deprivation, which was associated with the inhibition of caspase-9 and caspase-3 cleavages. It was reported that Pls content decreased in the brain of the Alzheimer's patients, which indicated that the reduction of Pls content could endanger neurons. The present findings, taken together, suggest that Pls have an anti-apoptotic action in the brain. Further studies on precise mechanisms of Pls-mediated protection against cell death may lead us to establish a novel therapeutic approach to cure neurodegenerative disorders. © 2013 Hossain et al.


Patent
Fujino Brain Research Co., Umeda Jimusho Ltd. and Marudai Food Co. | Date: 2011-09-22

An objective of the present invention is to provide a novel method with an effect of alleviating central nervous system inflammation. The present invention provides a drug against central nervous system inflammation containing a plasmalogen. More preferably, the present invention provides a drug against central nervous system inflammation containing a plasmalogen extracted from a biological tissue (preferably an avian tissue) that mainly contains an ethanolamine plasmalogen and a choline plasmalogen.


Patent
Marudai Food Co. | Date: 2012-11-14

An objective of the present invention is to provide a new substance having a cerebral nerve cell neogenesis effect. Another objective is to provide a cerebral nerve cell neogenesis agent that is effective in treating and/or preventing neurological disorders utilizing the substance. With the present invention, a cerebral nerve cell neogenesis agent containing a plasmalogen as an active ingredient is provided. In particular, a preferable cerebral nerve cell neogenesis agent contains, as an active ingredient, a biological tissue (preferably, an avian tissue) extracted plasmalogen mainly including an ethanolamine plasmalogen and a choline plasmalogen.


Patent
Fujino Brain Research Co., Marudai Food Co. and Umeda Jimusho Ltd. | Date: 2013-07-31

An objective of the present invention is to provide a novel method with an effect of alleviating central nervous system inflammation. The present invention provides a drug against central nervous system inflammation containing a plasmalogen. More preferably, the present invention provides a drug against central nervous system inflammation containing a plasmalogen extracted from a biological tissue (preferably an avian tissue) that mainly contains an ethanolamine plasmalogen and a choline plasmalogen.


This invention provides a process for producing a high-purity sphingomyelin and a high-purity plasmalogen-form glycerophospholipid from a biological material by simple procedures at high yields. The process comprises the steps of: (A) subjecting dried total lipids extracted from a biological material to extraction treatment with a specific mixture solution to separate an insoluble portion composed mainly of sphingomyelin and a soluble portion; (B) subjecting the insoluble portion, obtained in said Step (A), to washing treatment with a specific mixture solution to obtain crude sphingomyelin; (C) subjecting the soluble portion, obtained in said Step (A), to washing treatment with a water-soluble ketone solvent to obtain crude plasmalogen-form glycerophospholipid; (D) causing an enzyme to act on the crude sphingomyelin, obtained in said Step (B), to obtain sphingomyelin having a purity of 90% or more; and (E) causing an enzyme to act on the crude plasmalogen-form glycerophospholipid, obtained in said Step (C), to obtain plasmalogen-form glycerophospholipid having a purity of 40% or more.


PubMed | Kyushu University and Marudai Food Co.
Type: Journal Article | Journal: PloS one | Year: 2013

Neuronal cells are susceptible to many stresses, which will cause the apoptosis and neurodegenerative diseases. The precise molecular mechanism behind the neuronal protection against these apoptotic stimuli is necessary for drug discovery. In the present study, we have found that plasmalogens (Pls), which are glycerophospholipids containing vinyl ether linkage at sn-1 position, can protect the neuronal cell death upon serum deprivation. Interestingly, caspse-9, but not caspase-8 and caspase-12, was cleaved upon the serum starvation in Neuro-2A cells. Pls treatments effectively reduced the activation of caspase-9. Furthermore, cellular signaling experiments showed that Pls enhanced phosphorylation of the phosphoinositide 3-kinase (PI3K)-dependent serine/threonine-specific protein kinase AKT and extracellular-signal-regulated kinases ERK1/2. PI3K/AKT inhibitor LY294002 and MAPK/ERK kinase (MEK) inhibitor U0126 treatments study clearly indicated that Pls-mediated cell survival was dependent on the activation of these kinases. In addition, Pls also inhibited primary mouse hippocampal neuronal cell death induced by nutrient deprivation, which was associated with the inhibition of caspase-9 and caspase-3 cleavages. It was reported that Pls content decreased in the brain of the Alzheimers patients, which indicated that the reduction of Pls content could endanger neurons. The present findings, taken together, suggest that Pls have an anti-apoptotic action in the brain. Further studies on precise mechanisms of Pls-mediated protection against cell death may lead us to establish a novel therapeutic approach to cure neurodegenerative disorders.

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