AIM: To investigate if sleep deprivation is able to increase the expression of inducible heat shock protein 70 in gastric mucosa and its possible role in mucosal defense. METHODS: Rats for sleep disruption were placed...AIM: To investigate if sleep deprivation is able to increase the expression of inducible heat shock protein 70 in gastric mucosa and its possible role in mucosal defense. METHODS: Rats for sleep disruption were placed inside a computerized rotating drum, gastric mucosa was taken from rats with 1, 3 and 7d sleep deprivation. RT-PCR, immunohistochemistry and Western blotting were used to determine the expression of heat shock protein 70. Ethanol (500mL.L(-1), i.g.) was used to induce gastric mucosa damage. RESULTS: RT-PCR, Western blotting and immunostaining confirmed that the sleep deprivation as a stress resulted in significantly greater expression of inducible heat shock protein 70 in gastric mucosa of rats. After the 500mL.L(-1) ethanol challenge, the ulcer area found in the rats with 7d sleep deprivation (19.15 +/- 4.2)mm(2) was significantly lower (P【0.01) than the corresponding control (53.7 +/- 8.1) mm(2). CONCLUSION: Sleep deprivation as a stress, in addition to lowering the gastric mucosal barrier, is able to stimulate the expression of inducible heat shock protein 70 in gastric mucosa of rats, the heat shock protein 70 may play an important role in gastric mucosal protection.展开更多
AIM:The rote of the sphincter of Oddi(SO)in ethanol (ETOH)-induced pancreatitis is controversial.Our aim was to characterise the effect of E-I-OH on basal and stimulated SO motility. METHODS:SOs removed from white rab...AIM:The rote of the sphincter of Oddi(SO)in ethanol (ETOH)-induced pancreatitis is controversial.Our aim was to characterise the effect of E-I-OH on basal and stimulated SO motility. METHODS:SOs removed from white rabbits were placed in an organ bath(Krebs solution,pH7.4,37℃).The effects of 2 mL/L,4 mL/L,6 mL/L and 8 mL/L of ETOH on the contractile responses of the sphincter were determined. SOs were stimulated with either 0.1 μmol/L carbachol,1 μmol/L erythromycin or 0.1 μmol/L cholecystokinin(CCK). RESULTS:ETOH at a dose of 4 mL/L significantly decreased the baseline contractile amplitude from 11.98±0.05 mN to 11.19±0.07 mN.However,no significant changes in the contractile frequency were observed.ETOH(0.6%) significantly decreased both the baseline amplitude and the frequency compared to the control group(10.50±0.01 mN, 12.13±0.10 mN and 3.53±0.13 c/min,5.5±0.13 cycles(c)/min, respectively).Moreover,0.8% of ETOH resulted in complete relaxation of the SO.Carbachol(0.1 μmol/L)or erythromycin (1 μmol/L)stimulated the baseline amplitudes(by 82% and 75%,respectively)and the contractile frequencies (by 150% and 106%,respectively).In the carbachol or erythromydn-stimulated groups 2-6 mL/L of E-IOH significantly inhibited both the amplitude and the frequency.Interestingly, a 4-5 min administration of 6 mL/L ETOH suddenly and completely relaxed the SO.CCK(0.1 μmol/L)stimulated the baseline amplitude from 12.37±0.05 mN to 27.40±1.82 mN within 1.60±0.24 min.After this peak,the amplitude decreased to 17.17±0.22 mN and remained constant during the experiment.The frequency peaked at 12.8±0.2 c/min, after which the constant frequency was 9.43±0.24 c/min throughout the rest of the experiment.ETOH at a dose of 4 mL/L significantly decreased the amplitude from 16.13±0.23 mN to 14.93±0.19 mN.However,no significant changes in the contractile frequency were observed.ETOH at a dose of 6 mL/L inhibited both the amplitudes and the frequencies in the CCK-stimulated group,while 8 mL/L of ETOH completely relaxed the展开更多
目的:基于"上调MDR(multiple drug resistance)基因、诱导P-糖蛋白(P-gp,P-glycoprotein)外向转运解除中枢抑制药物中毒"的机制研究,对临床中毒多发的中枢抑制药物建立P-gp底物谱,明确适合该解救治疗方案的药物(毒物)。方法:...目的:基于"上调MDR(multiple drug resistance)基因、诱导P-糖蛋白(P-gp,P-glycoprotein)外向转运解除中枢抑制药物中毒"的机制研究,对临床中毒多发的中枢抑制药物建立P-gp底物谱,明确适合该解救治疗方案的药物(毒物)。方法:采用三磷酸腺苷酶(adenosine triphosphate,ATP)酶活性测试法确定待测中枢抑制药物是否为P-gp的底物。结果:舒必利、齐拉西酮、佐匹克隆、氯米帕明、西酞普兰及吗氯贝胺均为P-gp底物。舒必利、齐拉西酮与西酞普兰为非浓度依赖的ATP酶抑制剂,佐匹克隆、氯米帕明与吗氯贝胺浓度依赖的ATP酶双向调节子。结论:该研究结果将为新的中枢药物中毒解救方案的临床应用提供参考和依据。展开更多
文摘AIM: To investigate if sleep deprivation is able to increase the expression of inducible heat shock protein 70 in gastric mucosa and its possible role in mucosal defense. METHODS: Rats for sleep disruption were placed inside a computerized rotating drum, gastric mucosa was taken from rats with 1, 3 and 7d sleep deprivation. RT-PCR, immunohistochemistry and Western blotting were used to determine the expression of heat shock protein 70. Ethanol (500mL.L(-1), i.g.) was used to induce gastric mucosa damage. RESULTS: RT-PCR, Western blotting and immunostaining confirmed that the sleep deprivation as a stress resulted in significantly greater expression of inducible heat shock protein 70 in gastric mucosa of rats. After the 500mL.L(-1) ethanol challenge, the ulcer area found in the rats with 7d sleep deprivation (19.15 +/- 4.2)mm(2) was significantly lower (P【0.01) than the corresponding control (53.7 +/- 8.1) mm(2). CONCLUSION: Sleep deprivation as a stress, in addition to lowering the gastric mucosal barrier, is able to stimulate the expression of inducible heat shock protein 70 in gastric mucosa of rats, the heat shock protein 70 may play an important role in gastric mucosal protection.
基金Supported by The Wellcome Trust (Grant No.022618),and by the Hungarian Scientific Research Fund (D42188,T43066 and T042589)
文摘AIM:The rote of the sphincter of Oddi(SO)in ethanol (ETOH)-induced pancreatitis is controversial.Our aim was to characterise the effect of E-I-OH on basal and stimulated SO motility. METHODS:SOs removed from white rabbits were placed in an organ bath(Krebs solution,pH7.4,37℃).The effects of 2 mL/L,4 mL/L,6 mL/L and 8 mL/L of ETOH on the contractile responses of the sphincter were determined. SOs were stimulated with either 0.1 μmol/L carbachol,1 μmol/L erythromycin or 0.1 μmol/L cholecystokinin(CCK). RESULTS:ETOH at a dose of 4 mL/L significantly decreased the baseline contractile amplitude from 11.98±0.05 mN to 11.19±0.07 mN.However,no significant changes in the contractile frequency were observed.ETOH(0.6%) significantly decreased both the baseline amplitude and the frequency compared to the control group(10.50±0.01 mN, 12.13±0.10 mN and 3.53±0.13 c/min,5.5±0.13 cycles(c)/min, respectively).Moreover,0.8% of ETOH resulted in complete relaxation of the SO.Carbachol(0.1 μmol/L)or erythromycin (1 μmol/L)stimulated the baseline amplitudes(by 82% and 75%,respectively)and the contractile frequencies (by 150% and 106%,respectively).In the carbachol or erythromydn-stimulated groups 2-6 mL/L of E-IOH significantly inhibited both the amplitude and the frequency.Interestingly, a 4-5 min administration of 6 mL/L ETOH suddenly and completely relaxed the SO.CCK(0.1 μmol/L)stimulated the baseline amplitude from 12.37±0.05 mN to 27.40±1.82 mN within 1.60±0.24 min.After this peak,the amplitude decreased to 17.17±0.22 mN and remained constant during the experiment.The frequency peaked at 12.8±0.2 c/min, after which the constant frequency was 9.43±0.24 c/min throughout the rest of the experiment.ETOH at a dose of 4 mL/L significantly decreased the amplitude from 16.13±0.23 mN to 14.93±0.19 mN.However,no significant changes in the contractile frequency were observed.ETOH at a dose of 6 mL/L inhibited both the amplitudes and the frequencies in the CCK-stimulated group,while 8 mL/L of ETOH completely relaxed the
文摘目的:基于"上调MDR(multiple drug resistance)基因、诱导P-糖蛋白(P-gp,P-glycoprotein)外向转运解除中枢抑制药物中毒"的机制研究,对临床中毒多发的中枢抑制药物建立P-gp底物谱,明确适合该解救治疗方案的药物(毒物)。方法:采用三磷酸腺苷酶(adenosine triphosphate,ATP)酶活性测试法确定待测中枢抑制药物是否为P-gp的底物。结果:舒必利、齐拉西酮、佐匹克隆、氯米帕明、西酞普兰及吗氯贝胺均为P-gp底物。舒必利、齐拉西酮与西酞普兰为非浓度依赖的ATP酶抑制剂,佐匹克隆、氯米帕明与吗氯贝胺浓度依赖的ATP酶双向调节子。结论:该研究结果将为新的中枢药物中毒解救方案的临床应用提供参考和依据。
