Yeast-Derived β-Glucan Reduces Intestinal Injury in Rat Model of Necrotizing Enterocolitis

ثبت نشده
چکیده

β(1-3)-D-Glucan’s (glucans) are natural products found in yeast, mushrooms, grains and seaweed. β-Glucans represent a group of heterogeneous polysaccharides (both chemically and physicochemically) with strong immunomodulatory capabilities. Natural glucans are found mainly in whole grains, yeast, and mushroom. They represent a complex group of chemically heteregenous polysaccharides with significant immunomodulatory activities. Glucans are available in many dietary supplements; therefore, they can be easily used as complementary and alternative medicine. In addition to many animal studies where glucans were found to be active in a wide range of species (basically from shrimp to horses) the effects of glucans have been also examined in humans. Recently, a series of clinical studies showed strong effects on the treatment of children with chronic respiratory problems [1,2].

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Recombinant Human Trefoil Factor 3 Ameliorates Bowel Injury: Its Anti-Inflammatory Effect on Experimental Necrotizing Enterocolitis

Aim. Recombinant human trefoil factor 3 (intestinal trefoil factor) has been suggested to be partially protective against necrotizing enterocolitis (NEC), but the mechanisms of this protection have not been defined. We investigated whether the protective effects of rhTFF3 are the result of an anti-inflammatory response. Methods. The rats were killed on day 4, the distal ileum was harvested for ...

متن کامل

Bifidobacterium bifidum reduces apoptosis in the intestinal epithelium in necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is a devastating intestinal disease of neonates, and clinical studies suggest the beneficial effect of probiotics in NEC prevention. Recently, we have shown that administration of Bifidobacterium bifidum protects against NEC in a rat model. Intestinal apoptosis can be suppressed by activation of cyclooxygenase-2 (COX-2) and increased production of prostaglandin E...

متن کامل

Epidermal growth factor reduces autophagy in intestinal epithelium and in the rat model of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is a devastating intestinal disease of premature infants. Epidermal growth factor (EGF) is one of the most promising candidates in NEC prophylaxis. Autophagy regulates cell homeostasis, but uncontrolled activation of autophagy may lead to cellular injury. The aim was to evaluate the effects of EGF on intestinal autophagy in epithelial cells and in the rat NEC mod...

متن کامل

Lactobacillus bulgaricus prevents intestinal epithelial cell injury caused by Cronobacter 1 ( Enterobacter ) sakazakii - induced nitric oxide both in vitro and in the newborn rat model of 2 necrotizing enterocolitis . 3

Lactobacillus bulgaricus prevents intestinal epithelial cell injury caused by Cronobacter 1 (Enterobacter) sakazakii-induced nitric oxide both in vitro and in the newborn rat model of 2 necrotizing enterocolitis. 3 Catherine J. Hunter 1 , Monica Williams 1 , Mikael Petrosyan 1 , Yigit Guner 1 , Rahul Mittal 2 , Dennis 4 Mock 3 , Jeffrey S. Upperman 1, 4 , Henri R. Ford 1, 4 and Nemani V. Prasad...

متن کامل

Temporal profile of intestinal tissue expression of intestinal fatty acid-binding protein in a rat model of necrotizing enterocolitis

OBJECTIVES Necrotizing enterocolitis is a severe multifactorial intestinal disorder that primarily affects preterm newborns, causing 20-40% mortality and morbidity. Intestinal fatty acid-binding protein has been reported to be a biomarker for the detection of intestinal injuries. Our aim was to assess intestinal tissue injury and the molecular expression of intestinal fatty acid-binding protein...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2015