AIM: To study the role of gastric mucosal ascorbic acid(AA) in the progression of acute gastric mucosal lesions induced by compound 48/80 (C48/80), a mast cell degranulator, in rats.METHODS: C48/80 (0.75 mg/kg) was in...AIM: To study the role of gastric mucosal ascorbic acid(AA) in the progression of acute gastric mucosal lesions induced by compound 48/80 (C48/80), a mast cell degranulator, in rats.METHODS: C48/80 (0.75 mg/kg) was intraperitoneally injected to fasted Wistar rats. Oral administration of AA (10, 50 or 100 mg/kg) was performed 0.5 h after C48/80treatment. Determinations for gastric mucosal lesion severity and blood flow, and assays for gastric mucosal total AA, reduced AA, oxidized AA, vitamin E, thiobarbituric acid reactive substances (TBARS), adherent mucus, nitrite/nitrate (NOx), non-protein SH (NPSH), and myeloperoxidase(MPO), and serum total AA, reduced AA, oxidized AA,and NOx were conducted 0.5 and 3 h after C48/80treatment.RESULTS: Gastric mucosal lesions occurred 0.5 h after C48/80 treatment and progressed at 3 h. Gastric mucosal blood flow decreased 0.5 h after C48/80 treatment but the decrease was recovered at 3 h. Gastric mucosal total AA, reduced AA, vitamin E, and adherent mucus concentrations decreased 3 h after C48/80 treatment.Gastric mucosal oxidized AA concentration remained unchanged after C48/80 treatment. Gastric mucosal NPSH concentration decreased 0.5 h after C48/80 treatment,but the decrease was recovered at 3 h. Gastric mucosal TBARS concentration and MPO activity increased 0.5 h after C48/80 treatment and further increased at 3 h.Serum total AA and reduced AA concentrations increased 0.5 h after C48/80 treatment and further increased at 3 h, while serum oxidized AA concentration increased at 0.5 h. Serum and gastric mucosal NOx concentrations increased 3 h after C48/80 treatment. AA administration to C48/80-treated rats at 0.5 h after the treatment prevented the gastric mucosal lesion progression and the changes in gastric mucosal total AA, reduced AA, vitamin E, adherent mucus, NOx, and TBARS concentrations and MPO activity and serum NOx concentration found at 3 h after the treatment dose-dependently. The AA administration to C48/80-treated rats caused further increases in serum total AA and reduced AA concentrations at 3 h after the treatment dose-dependently.CONCLUSION: Gastric mucosal AA plays a critical role in the progression of C48/80-induced acute gastric mucosal lesions in rats.展开更多
Intestinal ischemia occurs in a wide variety of clinical manifestations. The gut barrier is broken down by bacterial translocation after small intestinal ischemia reperfusion injury （IIRI）, which can result in many ...Intestinal ischemia occurs in a wide variety of clinical manifestations. The gut barrier is broken down by bacterial translocation after small intestinal ischemia reperfusion injury （IIRI）, which can result in many clinical consequences, even death. The intestinal mucosal mast cells （IMMCs） serve as a unique cellular source of large amounts of vasoactive mediators, and they can influence local tissue reactions. We and others have previously shown that IIRI could activate IMMCs, make them degranulate and release a mass of inflammatory mediators, which in turn aggravate IIRI.展开更多
OBJECTIVE:To investigate the gastroprotective effects of Acanthopanax senticosus leaves(ASLs)extrusion on acute gastric mucosal lesion in rats induced by compound 48/80(C48/80).METHODS:Rats were divided into six group...OBJECTIVE:To investigate the gastroprotective effects of Acanthopanax senticosus leaves(ASLs)extrusion on acute gastric mucosal lesion in rats induced by compound 48/80(C48/80).METHODS:Rats were divided into six groups:normal;C48/80-induced gastric lesion control;gastric lesion positive control(famotidine 4 mg/kg);gastric lesion administered with two levels of extruded ASLs(ASLE,40 and 200 mg/kg);and gastric lesion treated with ASLs(ASL 200 mg/kg).Mucus secretion/damage was determined by immunohistological staining.Immunofluorescence and western blotting were performed to determine gastric mucosal Bax and Bcl-2 expression.Gastric mucosal oxidative-stress-related enzymes and malondialdehyde were determined.RESULTS:C48/80-induced mucus depletion and inflammation in the gastric mucosa were significantly attenuated by ASLs.The increased serum serotonin and histamine concentrations in C48/80-treated rats were also attenuated by ASLs.Gastric mucosal Bax protein expression was increased and Bcl-2 expression was decreased after C48/80 treatment,and ASLs ameliorated Bax and Bcl-2 expression.The extrusion process significantly augmented the effects of ASLs in a dosedependent manner.ASLEs at 200 mg/kg normalized mucus damage/secretion,C48/80-induced increases of mucosal myeloperoxidase activity(index of inflammation),xanthine oxidase,and malondialdehyde content(index of lipid peroxidation).The effects of ASLs on Bax and Bcl-2expression were also enhanced by extrusion.Furthermore,these effects of ASLEs at 200 mg/kg were similar to those of famotidine,a histamine H2-receptor antagonist commonly used to treat gastric ulcers.CONCLUSION:ASLEs prevented acute gastric mucosal lesion progression induced by C48/80,possibly by inducing mucus production,and reduced inflammation and oxidative stress in gastric mucosa through an anti-apoptotic mechanism.展开更多
Ni80Fe20/Ni48Fe12Cr40 bilayer films and Ni80Fe20 monolayer films were deposited at room temperature on SiO2/Si（100） substrates by electron beam evaporation. The influence of the thickness of the Ni48Fe12Cr40 underla...Ni80Fe20/Ni48Fe12Cr40 bilayer films and Ni80Fe20 monolayer films were deposited at room temperature on SiO2/Si（100） substrates by electron beam evaporation. The influence of the thickness of the Ni48Fe12Cr40 underlayer on the structure, magnetization, and magnetoresistance of the Ni80Fe20/Ni48Fe12Cr40 bilayer film was investigated. The thickness of the Ni48Fe12Cr40 layer varied from about 1 nm to 18 nm while the Ni80Fe20 layer thickness was fixed at 45 nm. For the as-deposited bilayer films the introducing of the Ni48Fe12Cr40 underlayer promotes both the （111） texture and grain growth in the Ni80Fe20 layer. The Ni48Fe12Cr40 underlayer has no significant influence on the magnetic moment of the Ni80Fe20/Ni48Fe12Cr40 bilayer film. However, the coercivity of the bilayer film changes with the thickness of the Ni48Fe12Cr40 undedayer. The optimum thickness of the Ni48Fe12Cr40 underlayer for improving the anisotropic magnetoresistance effect of the Ni80Fe20/Ni48Fe12Cr40 bilayer film is about 5 nm. With a decrease in temperature from 300 K to 81 K, the anisotropic magnetoresistance ratio of the Ni80Fe20 （45 nm）/Ni48Fe12Cr40 （5 nm） bilayer film increases linearly from 2.1% to 4.8% compared with that of the Ni80Fe20 monolayer film from 1.7% to 4.0%.展开更多
文摘AIM: To study the role of gastric mucosal ascorbic acid(AA) in the progression of acute gastric mucosal lesions induced by compound 48/80 (C48/80), a mast cell degranulator, in rats.METHODS: C48/80 (0.75 mg/kg) was intraperitoneally injected to fasted Wistar rats. Oral administration of AA (10, 50 or 100 mg/kg) was performed 0.5 h after C48/80treatment. Determinations for gastric mucosal lesion severity and blood flow, and assays for gastric mucosal total AA, reduced AA, oxidized AA, vitamin E, thiobarbituric acid reactive substances (TBARS), adherent mucus, nitrite/nitrate (NOx), non-protein SH (NPSH), and myeloperoxidase(MPO), and serum total AA, reduced AA, oxidized AA,and NOx were conducted 0.5 and 3 h after C48/80treatment.RESULTS: Gastric mucosal lesions occurred 0.5 h after C48/80 treatment and progressed at 3 h. Gastric mucosal blood flow decreased 0.5 h after C48/80 treatment but the decrease was recovered at 3 h. Gastric mucosal total AA, reduced AA, vitamin E, and adherent mucus concentrations decreased 3 h after C48/80 treatment.Gastric mucosal oxidized AA concentration remained unchanged after C48/80 treatment. Gastric mucosal NPSH concentration decreased 0.5 h after C48/80 treatment,but the decrease was recovered at 3 h. Gastric mucosal TBARS concentration and MPO activity increased 0.5 h after C48/80 treatment and further increased at 3 h.Serum total AA and reduced AA concentrations increased 0.5 h after C48/80 treatment and further increased at 3 h, while serum oxidized AA concentration increased at 0.5 h. Serum and gastric mucosal NOx concentrations increased 3 h after C48/80 treatment. AA administration to C48/80-treated rats at 0.5 h after the treatment prevented the gastric mucosal lesion progression and the changes in gastric mucosal total AA, reduced AA, vitamin E, adherent mucus, NOx, and TBARS concentrations and MPO activity and serum NOx concentration found at 3 h after the treatment dose-dependently. The AA administration to C48/80-treated rats caused further increases in serum total AA and reduced AA concentrations at 3 h after the treatment dose-dependently.CONCLUSION: Gastric mucosal AA plays a critical role in the progression of C48/80-induced acute gastric mucosal lesions in rats.
文摘Intestinal ischemia occurs in a wide variety of clinical manifestations. The gut barrier is broken down by bacterial translocation after small intestinal ischemia reperfusion injury （IIRI）, which can result in many clinical consequences, even death. The intestinal mucosal mast cells （IMMCs） serve as a unique cellular source of large amounts of vasoactive mediators, and they can influence local tissue reactions. We and others have previously shown that IIRI could activate IMMCs, make them degranulate and release a mass of inflammatory mediators, which in turn aggravate IIRI.
基金Supported by Cooperative Research Program for Agriculture Science and Technology Development and Rural Development Administration,Republic of Korea(Investigation of Functional Nutrients from Agricultural Food and Development of Integrated Information,No.PJ011644)
文摘OBJECTIVE:To investigate the gastroprotective effects of Acanthopanax senticosus leaves(ASLs)extrusion on acute gastric mucosal lesion in rats induced by compound 48/80(C48/80).METHODS:Rats were divided into six groups:normal;C48/80-induced gastric lesion control;gastric lesion positive control(famotidine 4 mg/kg);gastric lesion administered with two levels of extruded ASLs(ASLE,40 and 200 mg/kg);and gastric lesion treated with ASLs(ASL 200 mg/kg).Mucus secretion/damage was determined by immunohistological staining.Immunofluorescence and western blotting were performed to determine gastric mucosal Bax and Bcl-2 expression.Gastric mucosal oxidative-stress-related enzymes and malondialdehyde were determined.RESULTS:C48/80-induced mucus depletion and inflammation in the gastric mucosa were significantly attenuated by ASLs.The increased serum serotonin and histamine concentrations in C48/80-treated rats were also attenuated by ASLs.Gastric mucosal Bax protein expression was increased and Bcl-2 expression was decreased after C48/80 treatment,and ASLs ameliorated Bax and Bcl-2 expression.The extrusion process significantly augmented the effects of ASLs in a dosedependent manner.ASLEs at 200 mg/kg normalized mucus damage/secretion,C48/80-induced increases of mucosal myeloperoxidase activity(index of inflammation),xanthine oxidase,and malondialdehyde content(index of lipid peroxidation).The effects of ASLs on Bax and Bcl-2expression were also enhanced by extrusion.Furthermore,these effects of ASLEs at 200 mg/kg were similar to those of famotidine,a histamine H2-receptor antagonist commonly used to treat gastric ulcers.CONCLUSION:ASLEs prevented acute gastric mucosal lesion progression induced by C48/80,possibly by inducing mucus production,and reduced inflammation and oxidative stress in gastric mucosa through an anti-apoptotic mechanism.
文摘Ni80Fe20/Ni48Fe12Cr40 bilayer films and Ni80Fe20 monolayer films were deposited at room temperature on SiO2/Si（100） substrates by electron beam evaporation. The influence of the thickness of the Ni48Fe12Cr40 underlayer on the structure, magnetization, and magnetoresistance of the Ni80Fe20/Ni48Fe12Cr40 bilayer film was investigated. The thickness of the Ni48Fe12Cr40 layer varied from about 1 nm to 18 nm while the Ni80Fe20 layer thickness was fixed at 45 nm. For the as-deposited bilayer films the introducing of the Ni48Fe12Cr40 underlayer promotes both the （111） texture and grain growth in the Ni80Fe20 layer. The Ni48Fe12Cr40 underlayer has no significant influence on the magnetic moment of the Ni80Fe20/Ni48Fe12Cr40 bilayer film. However, the coercivity of the bilayer film changes with the thickness of the Ni48Fe12Cr40 undedayer. The optimum thickness of the Ni48Fe12Cr40 underlayer for improving the anisotropic magnetoresistance effect of the Ni80Fe20/Ni48Fe12Cr40 bilayer film is about 5 nm. With a decrease in temperature from 300 K to 81 K, the anisotropic magnetoresistance ratio of the Ni80Fe20 （45 nm）/Ni48Fe12Cr40 （5 nm） bilayer film increases linearly from 2.1% to 4.8% compared with that of the Ni80Fe20 monolayer film from 1.7% to 4.0%.
