AIM： To evaluate the gastro-protective effect of capsaicin against the ethanol- and indomethacin （IND）-induced gastric mucosal damage in healthy human subjects. METHODS： The effects of small doses （1-8 μg/mL, 10...AIM： To evaluate the gastro-protective effect of capsaicin against the ethanol- and indomethacin （IND）-induced gastric mucosal damage in healthy human subjects. METHODS： The effects of small doses （1-8 μg/mL, 100 mL） of capsaicin on the gastric acid secretion basal acid output （BAO） and its electrolyte concentration, gastric transmucosal potential difference （GTPD）, ethanol- （5 mL 300 mL/L i.g.） and IND- （3×25 mg/d） induced gastric mucosal damage were tested in a randomized, prospective study of 84 healthy human subjects. The possible role of desensitization of capsaicin-sensitive afferents was tested by repeated exposures and during a prolonged treatment. RESULTS： Intragastric application of capsaicin decreased the BAO and enhanced “non-parietal” component, GTPD in a dose-dependent manner. The decrease of GTPD evoked by ethanol was inhibited by the capsaicin application, which was reproducible. Gastric microbleeding induced by IND was inhibited by co-administration with capsaicin, but was not influenced by two weeks pretreatment with a daily capsaicin dose of 3×400μg i.g. CONCLUSION： Capsaicin in low concentration range protects against gastric injuries induced by ethanol or IND, which is attributed to stimulation of the sensory nerve endings.展开更多
AIM： To investigate the effects of curcumin on gastric microcirculation and inflammation in rats with indo- methacin-induced gastric damage. METHODS： Male Sprague-Dawley rats were randomly divided into three groups....AIM： To investigate the effects of curcumin on gastric microcirculation and inflammation in rats with indo- methacin-induced gastric damage. METHODS： Male Sprague-Dawley rats were randomly divided into three groups. Group 1 （control group, n = 5） was fed with olive oil and 5% NaHCOf （vehicle）. Group 2 [indomethacin （IMN） group, n = 5] was fed with olive oil 30 min prior to indomethacin 150 mg/kg body weight （BW） dissolved in 5% NaHCO3- at time 0th and 4th h. Group 3 （INN ± Cur group, n = 4） was fed with curcumin 200 mg/kg BW dissolved in olive oil 0.5 mL, 30 min prior to indomethacin at 0th and 4th h. Leukocyte-endothelium interactions at postcapillary venules were recorded after acridine orange injection. Blood samples were determined for intercellular ad- hesion molecule （ICAM）-1 and tumor necrosis factor （TNF）-a levels using enzyme linked immunosorbent assay method. Finally, the stomach was removed for histopathological examination for gastric lesions and grading for neutrophil infiltration. RESULTS： In group 2, the leukocyte adherence in postcapillary venules was significantly increased com- pared to the control group （6.40±2.30 cells/frame vs 1.20 ± 0.83 cells/frame, P = 0.001）. Pretreatment with curcumin caused leukocyte adherence to postcapil- lary venule to decline （3.00±0.81 cells/frame vs 6.40 ± 2.30 cells/frame, P = 0.027）. The levels of ICAM-1 and TNF-aincreased significantly in the indomethacin- treated group compared with the control group （1106.50 ± 504.22 pg/mL vs 336.93 a= 224.82 pg/mL, P = 0.011 and 230.92±114.47 pg/mL vs 47.13±65.59 pg/mL, P = 0.009 respectively）. Pretreatment with curcumin sig- nificantly decreased the elevation of ICAM-1 and TNF-a levels compared to treatment with indomethacin alone （413.66 ± 147.74 pg/mL vs 1106.50 ± 504.22 pg/mL, P = 0.019 and 58.27 ± 67.74 pg/mL vs 230.92 ± 114.47 pg/mL, P = 0.013 respectively）. The histological appear- ance of the stomach in the control group was normal. In the indomethacin-treated group, the stomachs showed a mild to moderate neutrophil infiltration score. Gastric lesions were erosive and ulcerative. In rats treated with indomethacin and curcumin, stomach histopathology improved and showed only a mild neutrophil infiltration score and fewer erosive lesions in the gastric mucosa. CONCLUSION： The results indicate that curcumin pre- vents indomethacin-induced gastropathy through the improvement of gastric microcirculation by attenuating the level of ICAM-1 and TNF-a,展开更多
AIM： To examine the anti-ulcerogenic and antioxidant effects of aqueous extracts of Foeniculum vu/gare （FVE） on ethanol-induced gastric lesions in rats.METHODS： FVE was administered by gavage at doses of 75, i50 a...AIM： To examine the anti-ulcerogenic and antioxidant effects of aqueous extracts of Foeniculum vu/gare （FVE） on ethanol-induced gastric lesions in rats.METHODS： FVE was administered by gavage at doses of 75, i50 and 300 mg/kg, and famotidine was used at the dose of20mg/kg.Following a 60 min period, all the rats were given 1 mL of ethanol （80%） by gavage. One hour after the administration of ethanol, all groups were sacrificed, and the gastric ulcer index was calculated; whole blood malondialdehyde （MDA） and reduced glutathione （GSH）, serum nitrate, nitrite, ascorbic acid, retinol and β-carotene levels were measured in all the groups.RESULTS： It was found that pretreatment with FVE significantly reduced ethanol-induced gastric damage. This effect of FVE was highest and statistically significant in 300 mg/kg group compared with the control （4.18 ± 2.81 vs 13.15 ± 4.08, P 〈 0.001）. Also, pretreatment with FVE significantly reduced the MDA levels, while significantly increased GSH, nitrite, nitrate, ascorbic acid, retinol and β-carotene levels. CONCLUSION： FVE has clearly a protective effect against ethanol-induced gastric mucosal lesion, and this effect, at least in part, depends upon the reduction in lipid peroxidation and augmentation in the antioxidant activity.展开更多
AIM： To evaluate the association between gastroesophageal reflux diseases （GERD） and coronary heart diseases. METHODS： One thousand nine hundred and seventy consecutive patients who attended our hospital were enro...AIM： To evaluate the association between gastroesophageal reflux diseases （GERD） and coronary heart diseases. METHODS： One thousand nine hundred and seventy consecutive patients who attended our hospital were enrolled. All of the patients who first attend our hospital were asked to respond to the F-scale questionnaire regardless of their chief complaints. All patients had a careful history taken, and resting echocardiography （ECG） was performed by physicians if the diagnostic necessity arose. Patients with ECG signs of coronary artery ischemia were defined as ST- segment depression based on the Minnesota code. RESULTS： Among 712 patients （36%） with GERD, ECG was performed in 171 （24%）, and ischemic changes were detected in eight （5%）. Four （50%） of these patients with abnormal findings upon ECG had no chest symptoms such as chest pain, chest oppression, or palpitations. These patients （0.6%; 4/712） were thought to have non-GERD heartburn, which may be related to ischemic heart disease. Of 281 patients who underwent ECG and did not have GERD symptoms, 20 （7%） had abnormal findings upon ECG. In patients with GERD symptoms and ECG signs of coronary artery ischemia, the prevalence of linked angina was considered to be 0.4% （8/1970 patients）.CONCLUSION： The present study suggested that ischemic heart disease might be found although a patient was referred to the hospital with a complaint of GERD symptoms. Physicians have to be concerned about missing clinically important coronary artery disease while evaluating patients for GERD symptoms.展开更多
The objective of this appraisal is to shed light on the various approaches to screen sensory information in the human gut. Understanding and characterization of sensory symptoms in gastrointestinal disorders is poor. ...The objective of this appraisal is to shed light on the various approaches to screen sensory information in the human gut. Understanding and characterization of sensory symptoms in gastrointestinal disorders is poor. Experimental methods allowing the investigator to control stimulus intensity and modality, as well as using validated methods for assessing sensory response have contributed to the understanding of pain mechanisms. Mechanical stimulation based on impedance planimetry allows direct recordings of luminal cross-sectional areas, and combined with ultrasound and magnetic resonance imaging, the contribution of different gut layers can be estimated. Electrical stimulation depolarizes free nerve endings non-selectively. Consequently, the stimulation paradigm （single, train, tetanic） influences the involved sensory nerves. Visual controlled electrical stimulation combines the probes with an endoscopic approach, which allows the investigator to inspect and obtain small biopsies from the stimulation site. Thermal stimulation （cold or warm） activates selectively mucosal receptors, and chemical substances such as acid and capsaicin （either alone or in combination） are used to evoke pain and sensitization. The possibility of multimodal （e.g. mechanical, electrical, thermal and chemical） stimulation in different gut segments has developed visceral pain research. The major advantage is involvement of distinctive receptors, various sensory nerves and different pain pathways mimicking clinical pain that favors investigation of central pain mechanisms involved in allodynia, hyperalgesia and referred pain. As impairment of descending control mechanisms partly underlies the pathogenesis in chronic pain, a cold pressor test that indirectly stimulates such control mechanisms can be added. Hence, the methods undoubtedly represent a major step forward in the future characterization and treatment of patients with various diseases of the gut, which provides knowledge to dinicians about the underlying symptoms and treatment of these patients.展开更多
文摘AIM： To evaluate the gastro-protective effect of capsaicin against the ethanol- and indomethacin （IND）-induced gastric mucosal damage in healthy human subjects. METHODS： The effects of small doses （1-8 μg/mL, 100 mL） of capsaicin on the gastric acid secretion basal acid output （BAO） and its electrolyte concentration, gastric transmucosal potential difference （GTPD）, ethanol- （5 mL 300 mL/L i.g.） and IND- （3×25 mg/d） induced gastric mucosal damage were tested in a randomized, prospective study of 84 healthy human subjects. The possible role of desensitization of capsaicin-sensitive afferents was tested by repeated exposures and during a prolonged treatment. RESULTS： Intragastric application of capsaicin decreased the BAO and enhanced “non-parietal” component, GTPD in a dose-dependent manner. The decrease of GTPD evoked by ethanol was inhibited by the capsaicin application, which was reproducible. Gastric microbleeding induced by IND was inhibited by co-administration with capsaicin, but was not influenced by two weeks pretreatment with a daily capsaicin dose of 3×400μg i.g. CONCLUSION： Capsaicin in low concentration range protects against gastric injuries induced by ethanol or IND, which is attributed to stimulation of the sensory nerve endings.
基金Supported by The Grant of Ratchadaphiseksomphot,Faculty of Medicine,Chulalongkorn University,Bangkok,Thailand[RA53/52(2)]
文摘AIM： To investigate the effects of curcumin on gastric microcirculation and inflammation in rats with indo- methacin-induced gastric damage. METHODS： Male Sprague-Dawley rats were randomly divided into three groups. Group 1 （control group, n = 5） was fed with olive oil and 5% NaHCOf （vehicle）. Group 2 [indomethacin （IMN） group, n = 5] was fed with olive oil 30 min prior to indomethacin 150 mg/kg body weight （BW） dissolved in 5% NaHCO3- at time 0th and 4th h. Group 3 （INN ± Cur group, n = 4） was fed with curcumin 200 mg/kg BW dissolved in olive oil 0.5 mL, 30 min prior to indomethacin at 0th and 4th h. Leukocyte-endothelium interactions at postcapillary venules were recorded after acridine orange injection. Blood samples were determined for intercellular ad- hesion molecule （ICAM）-1 and tumor necrosis factor （TNF）-a levels using enzyme linked immunosorbent assay method. Finally, the stomach was removed for histopathological examination for gastric lesions and grading for neutrophil infiltration. RESULTS： In group 2, the leukocyte adherence in postcapillary venules was significantly increased com- pared to the control group （6.40±2.30 cells/frame vs 1.20 ± 0.83 cells/frame, P = 0.001）. Pretreatment with curcumin caused leukocyte adherence to postcapil- lary venule to decline （3.00±0.81 cells/frame vs 6.40 ± 2.30 cells/frame, P = 0.027）. The levels of ICAM-1 and TNF-aincreased significantly in the indomethacin- treated group compared with the control group （1106.50 ± 504.22 pg/mL vs 336.93 a= 224.82 pg/mL, P = 0.011 and 230.92±114.47 pg/mL vs 47.13±65.59 pg/mL, P = 0.009 respectively）. Pretreatment with curcumin sig- nificantly decreased the elevation of ICAM-1 and TNF-a levels compared to treatment with indomethacin alone （413.66 ± 147.74 pg/mL vs 1106.50 ± 504.22 pg/mL, P = 0.019 and 58.27 ± 67.74 pg/mL vs 230.92 ± 114.47 pg/mL, P = 0.013 respectively）. The histological appear- ance of the stomach in the control group was normal. In the indomethacin-treated group, the stomachs showed a mild to moderate neutrophil infiltration score. Gastric lesions were erosive and ulcerative. In rats treated with indomethacin and curcumin, stomach histopathology improved and showed only a mild neutrophil infiltration score and fewer erosive lesions in the gastric mucosa. CONCLUSION： The results indicate that curcumin pre- vents indomethacin-induced gastropathy through the improvement of gastric microcirculation by attenuating the level of ICAM-1 and TNF-a,
文摘AIM： To examine the anti-ulcerogenic and antioxidant effects of aqueous extracts of Foeniculum vu/gare （FVE） on ethanol-induced gastric lesions in rats.METHODS： FVE was administered by gavage at doses of 75, i50 and 300 mg/kg, and famotidine was used at the dose of20mg/kg.Following a 60 min period, all the rats were given 1 mL of ethanol （80%） by gavage. One hour after the administration of ethanol, all groups were sacrificed, and the gastric ulcer index was calculated; whole blood malondialdehyde （MDA） and reduced glutathione （GSH）, serum nitrate, nitrite, ascorbic acid, retinol and β-carotene levels were measured in all the groups.RESULTS： It was found that pretreatment with FVE significantly reduced ethanol-induced gastric damage. This effect of FVE was highest and statistically significant in 300 mg/kg group compared with the control （4.18 ± 2.81 vs 13.15 ± 4.08, P 〈 0.001）. Also, pretreatment with FVE significantly reduced the MDA levels, while significantly increased GSH, nitrite, nitrate, ascorbic acid, retinol and β-carotene levels. CONCLUSION： FVE has clearly a protective effect against ethanol-induced gastric mucosal lesion, and this effect, at least in part, depends upon the reduction in lipid peroxidation and augmentation in the antioxidant activity.
文摘AIM： To evaluate the association between gastroesophageal reflux diseases （GERD） and coronary heart diseases. METHODS： One thousand nine hundred and seventy consecutive patients who attended our hospital were enrolled. All of the patients who first attend our hospital were asked to respond to the F-scale questionnaire regardless of their chief complaints. All patients had a careful history taken, and resting echocardiography （ECG） was performed by physicians if the diagnostic necessity arose. Patients with ECG signs of coronary artery ischemia were defined as ST- segment depression based on the Minnesota code. RESULTS： Among 712 patients （36%） with GERD, ECG was performed in 171 （24%）, and ischemic changes were detected in eight （5%）. Four （50%） of these patients with abnormal findings upon ECG had no chest symptoms such as chest pain, chest oppression, or palpitations. These patients （0.6%; 4/712） were thought to have non-GERD heartburn, which may be related to ischemic heart disease. Of 281 patients who underwent ECG and did not have GERD symptoms, 20 （7%） had abnormal findings upon ECG. In patients with GERD symptoms and ECG signs of coronary artery ischemia, the prevalence of linked angina was considered to be 0.4% （8/1970 patients）.CONCLUSION： The present study suggested that ischemic heart disease might be found although a patient was referred to the hospital with a complaint of GERD symptoms. Physicians have to be concerned about missing clinically important coronary artery disease while evaluating patients for GERD symptoms.
基金Supported by Det Obelske Familie fond and Spar Nord Fonden
文摘The objective of this appraisal is to shed light on the various approaches to screen sensory information in the human gut. Understanding and characterization of sensory symptoms in gastrointestinal disorders is poor. Experimental methods allowing the investigator to control stimulus intensity and modality, as well as using validated methods for assessing sensory response have contributed to the understanding of pain mechanisms. Mechanical stimulation based on impedance planimetry allows direct recordings of luminal cross-sectional areas, and combined with ultrasound and magnetic resonance imaging, the contribution of different gut layers can be estimated. Electrical stimulation depolarizes free nerve endings non-selectively. Consequently, the stimulation paradigm （single, train, tetanic） influences the involved sensory nerves. Visual controlled electrical stimulation combines the probes with an endoscopic approach, which allows the investigator to inspect and obtain small biopsies from the stimulation site. Thermal stimulation （cold or warm） activates selectively mucosal receptors, and chemical substances such as acid and capsaicin （either alone or in combination） are used to evoke pain and sensitization. The possibility of multimodal （e.g. mechanical, electrical, thermal and chemical） stimulation in different gut segments has developed visceral pain research. The major advantage is involvement of distinctive receptors, various sensory nerves and different pain pathways mimicking clinical pain that favors investigation of central pain mechanisms involved in allodynia, hyperalgesia and referred pain. As impairment of descending control mechanisms partly underlies the pathogenesis in chronic pain, a cold pressor test that indirectly stimulates such control mechanisms can be added. Hence, the methods undoubtedly represent a major step forward in the future characterization and treatment of patients with various diseases of the gut, which provides knowledge to dinicians about the underlying symptoms and treatment of these patients.
