Pruritus is an individual unpleasant sensation of human sensory nervous system. In the physiological condition it excerts a self-protective mechanism to protect the skin against external harmful agents. Pruritoceptive...Pruritus is an individual unpleasant sensation of human sensory nervous system. In the physiological condition it excerts a self-protective mechanism to protect the skin against external harmful agents. Pruritoceptive itch is also a major symptom of skin disease and a common reason for consulting a dermatologist in clinic. It has been well known that both histamine-dependent and histamine-independent pathways mediate acute and chronic itch sensations. Previous studies have showed common neural pathways partially shared by itch and pain sensation, and significant sex differences in pain sensation. However, sex difference in itch sensation has not been given too much attention as the majority of itch studies were done in male mice or rats till now. In the present study, we compared the scratching behaviors induced by pruritogenic agents in male and female C57BL/6 mice. The results showed that both males and females exhibited scratching behaviors in response to the intradermal injection of histamine-dependent and histamine-independent pruritogenic chemicals. Moreover, the number of scratching behaviors in response to compound 4880 and chloroquine were significantly higher in females. These results suggested that sex differences occured in histamine-dependent compound 4880-induced and histamine-independent chloroquine-induced itch sensations, but not in histamine-independent SLIGRL-NH2-induced itch sensation.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
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
Background Study of the relationship between mast cells and atherosclerosis is mostly dependent on pathological observation and cytology experiments. To investigate the effects of mast cells degranulation on plaque an...Background Study of the relationship between mast cells and atherosclerosis is mostly dependent on pathological observation and cytology experiments. To investigate the effects of mast cells degranulation on plaque and their possible mechanisms we used apolipoprotein E knockout mice which had been placed perivascular common carotid collar with mast cells degranulator compound 48-80. Methods Forty apolipoprotein E knockout mice were fed a western-type diet and operated on with placement of perivascular right common carotid collar. Four weeks after surgery, the mice were intraperitoneally injected with compound 48-80 （0.5 mg/kg） or D-Hanks every other day for 4 times. The serum lipids and activity of tryptase were measured. Tissue sections were stained with hematoxylin and eosin. Corresponding sections were stained with toluidine blue and immunohistochemically with antibodies against macrophage-specific antigen, a-smooth muscle actin, interleukin-1β and von Willebrand factor. Simultaneously, basic fibroblast growth factor was detected by in situ hybridization and immunofluorescence. Results No pathological change was observed in common carotid non-collar placement but atherogenesis in common carotid collar placement of both groups. There was a significant increase in plaque area （（5.85±0.75）×10^4 vs （0.86±0.28）×10^4 um^2, P 〈0.05）, the degree of lumen stenosis （（81±15）% vs （41±12）%, P 〈0.05）, the activity of tryptase in serum （（0.57±0.13） U/L vs （0.36±0.10） U/L, P 〈0.05）, and the percentage of degranulated mast cells （（80.6±17.8）% vs （13.5±4.1）%, P 〈0.05）. The expressions of macrophage-specific antigen, α-smooth muscle actin, interleukin-1β, basic fibroblast growth factor and the density of neovessel in plaque were more in the compound 48-80 group than in the control group. Conclusions Perivascular common carotid collar placement can promote atherosclerotic plaque formation in apolipoprotein E knockout mice. Compound 48-80 increases plaque area and the degree of lumen stenosis by the mechanism that compound 48-80 promotes proliferation of smooth muscle cells and aggregation of macrophages. Compound 48-80 promotes angiogenesis in plaque. The mechanism is potentially that compound 48-80 increases the expressions of basic fibroblast growth factor mRNA and protein in plaque. Compound 48-80 enhances the expression of interleukin-1β in plaque.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
文摘Pruritus is an individual unpleasant sensation of human sensory nervous system. In the physiological condition it excerts a self-protective mechanism to protect the skin against external harmful agents. Pruritoceptive itch is also a major symptom of skin disease and a common reason for consulting a dermatologist in clinic. It has been well known that both histamine-dependent and histamine-independent pathways mediate acute and chronic itch sensations. Previous studies have showed common neural pathways partially shared by itch and pain sensation, and significant sex differences in pain sensation. However, sex difference in itch sensation has not been given too much attention as the majority of itch studies were done in male mice or rats till now. In the present study, we compared the scratching behaviors induced by pruritogenic agents in male and female C57BL/6 mice. The results showed that both males and females exhibited scratching behaviors in response to the intradermal injection of histamine-dependent and histamine-independent pruritogenic chemicals. Moreover, the number of scratching behaviors in response to compound 4880 and chloroquine were significantly higher in females. These results suggested that sex differences occured in histamine-dependent compound 4880-induced and histamine-independent chloroquine-induced itch sensations, but not in histamine-independent SLIGRL-NH2-induced itch sensation.
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.
基金The study was supported by a grant from the National Natural Science Foundation of China （No. 30470720）.
文摘Background Study of the relationship between mast cells and atherosclerosis is mostly dependent on pathological observation and cytology experiments. To investigate the effects of mast cells degranulation on plaque and their possible mechanisms we used apolipoprotein E knockout mice which had been placed perivascular common carotid collar with mast cells degranulator compound 48-80. Methods Forty apolipoprotein E knockout mice were fed a western-type diet and operated on with placement of perivascular right common carotid collar. Four weeks after surgery, the mice were intraperitoneally injected with compound 48-80 （0.5 mg/kg） or D-Hanks every other day for 4 times. The serum lipids and activity of tryptase were measured. Tissue sections were stained with hematoxylin and eosin. Corresponding sections were stained with toluidine blue and immunohistochemically with antibodies against macrophage-specific antigen, a-smooth muscle actin, interleukin-1β and von Willebrand factor. Simultaneously, basic fibroblast growth factor was detected by in situ hybridization and immunofluorescence. Results No pathological change was observed in common carotid non-collar placement but atherogenesis in common carotid collar placement of both groups. There was a significant increase in plaque area （（5.85±0.75）×10^4 vs （0.86±0.28）×10^4 um^2, P 〈0.05）, the degree of lumen stenosis （（81±15）% vs （41±12）%, P 〈0.05）, the activity of tryptase in serum （（0.57±0.13） U/L vs （0.36±0.10） U/L, P 〈0.05）, and the percentage of degranulated mast cells （（80.6±17.8）% vs （13.5±4.1）%, P 〈0.05）. The expressions of macrophage-specific antigen, α-smooth muscle actin, interleukin-1β, basic fibroblast growth factor and the density of neovessel in plaque were more in the compound 48-80 group than in the control group. Conclusions Perivascular common carotid collar placement can promote atherosclerotic plaque formation in apolipoprotein E knockout mice. Compound 48-80 increases plaque area and the degree of lumen stenosis by the mechanism that compound 48-80 promotes proliferation of smooth muscle cells and aggregation of macrophages. Compound 48-80 promotes angiogenesis in plaque. The mechanism is potentially that compound 48-80 increases the expressions of basic fibroblast growth factor mRNA and protein in plaque. Compound 48-80 enhances the expression of interleukin-1β in plaque.
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.
