epiglucan has been researched along with Stomach-Ulcer* in 3 studies
3 other study(ies) available for epiglucan and Stomach-Ulcer
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Protective effects of β-glucan isolated from highland barley on ethanol-induced gastric damage in rats and its benefits to mice gut conditions.
Gastrointestinal tract disease is a global health problem which affects a major part of the world population. In this study, the gastroprotective effects of β-glucan isolated from highland barley on ethanol-induced gastric damage in rats and its benefits to mice gut health were investigated. Biochemical and pathological analysis methods were adopted to evaluating the gastrointestinal tract protective of β-glucan isolated from highland barley. In the ulceration model, it was found that β-glucan treatment could mitigate the gastric lesions and gastric mucosal damage caused by ethanol, decrease the gastric ulcer index. Furthermore, β-glucan treatment alleviated the gastric oxidative stress injury in vehicle rats through increasing the activity of superoxide dismutase and catalase, decreasing the level of malondialdehyde. In addition, β-glucan treatment also could decrease the level of interleukin-6 and tumor necrosis factor alpha and increased level of prostaglandin E2, nitric oxide. In the mouse gut health promoting model, β-glucan treatment increased the colon length, faces water contents and the concentration of total short-chain fatty acids (SCFAs) both in mice colon and cecum. Taken together, these results may indicate that β-glucan isolated from highland barley exert protective effects on the gastrointestinal tract of laboratory rodents. Topics: Animals; Antioxidants; beta-Glucans; Ethanol; Gastrointestinal Microbiome; Hordeum; Male; Mice; Oxidative Stress; Plant Extracts; Rats; Rats, Sprague-Dawley; Stomach; Stomach Ulcer | 2019 |
Protective effect of β-(1,3 → 1,6)-D-glucan against irritant-induced gastric lesions.
β-(1,3)-D-Glucan with β-(1,6) branches has been reported to have various pharmacological activities, such as anti-tumour and anti-infection activities, which result from its immunomodulating effects. Gastric lesions result from an imbalance between aggressive and defensive factors. In the present study, we examined the effect of β-(1,3)-D-glucan with β-(1,6) branches isolated from Aureobasidium pullulans on the gastric ulcerogenic response in mice. Oral administration of β-glucan ameliorated gastric lesions induced by ethanol (EtOH) or HCl. This administration of β-glucan also suppressed EtOH-induced inflammatory responses, such as infiltration of neutrophils and expression of pro-inflammatory cytokines, chemokines and cell adhesion molecules (CAM) at the gastric mucosa. Of the various defensive factors, the levels of heat shock protein (HSP) 70 and mucin but not PGE(2) were increased by the administration of β-glucan. β-Glucan-dependent induction of the expression of HSP70 and mucin proteins and suppression of the expression of pro-inflammatory cytokines, chemokines and CAM were also observed in cultured cells in vitro. The results of the present study suggest that β-glucan protects the gastric mucosa from the formation of irritant-induced lesions by increasing the levels of defensive factors, such as HSP70 and mucin. Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Carcinoma; Cell Adhesion Molecules; Cells, Cultured; Cytokines; Gastric Mucins; Gastric Mucosa; Gene Expression Regulation; Glucans; HSP70 Heat-Shock Proteins; Humans; Inflammation Mediators; Irritants; Macrophages, Peritoneal; Male; Mice; Mice, Inbred ICR; Neutrophil Infiltration; Protective Agents; RNA, Messenger; Stomach Neoplasms; Stomach Ulcer; Tumor Cells, Cultured | 2011 |
Protective effects of barley and its hydrolysates on gastric stress ulcer in rats.
This research intends to clarify the protective effect of barley and its hydrolysates with respect to a water immersion stress-induced ulcer in the rat model. The beta-(1-->3)-glucan content of barley, and specifically beta-(1-->4),(1-->3)-glucan content was determined and then gastric stress ulcerogenesis induced by water immersion was conducted using five-week-old male Sprague-Dawley rats (7 rats in one group). The barley diet group was fed 10% barley flour that was substituted with sucrose in the control diet. For the 3 groups fed on soluble dietary fiber (SDF), the diets were supplemented with 0.46 g of SDF, equivalent to 100 g of the control diet; 0.46 g of SDF is equivalent to 10 g of barley flour. The rats were housed in a stress-cage and immersed in a water bath (23 degrees C) up to their necks for 21 h. The content of SDF and beta-(1-->3)-glucan content in barley flour were 4.6% and 3.4%, respectively. Although strongly anti-ulcer activities were observed in the barley (10%), SDF isolated and beta-(1-->3)-glucan fraction (Hydrolysate I) prepared from barley flour after treatment with lichenase, in other words, beta-(1-->4),(1-->3)-glucan itself, its hydrolysate (Hydrolysate II) with beta-(1-->3)-glucosidase did not display any anti-ulcer activity. This finding suggests that the beta-(1-->3)-glucosyl-linkage on beta-(1-->3)-glucan is an important part of the active principle for anti-ulcerogenesis. Topics: Animals; beta-Glucans; Dietary Fiber; Disease Models, Animal; Food Analysis; Glucans; Hordeum; Immersion; Male; Rats; Rats, Sprague-Dawley; Solubility; Stomach Ulcer; Stress, Physiological | 2004 |