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柴胡总皂苷与16,16-二甲基前列腺素E2对单宁酸诱导的大鼠胃黏膜损伤影响的比较。

Comparison between the effects of crude saikosaponin and 16, 16-dimethyl prostaglandin E2 on tannic acid-induced gastric mucosal damage in rats.

作者信息

Hung C R, Wu T S, Chang T Y

机构信息

Department of Pharmacology, Medical College National Cheng Kung University Tainan, Taiwan, Republic of China.

出版信息

Chin J Physiol. 1993;36(4):211-7.

PMID:8020335
Abstract

Hung, C.R., T.S. Wu and T.Y. Chang. The comparison between the effects of ethanol-extracted saikosaponin (SS) and 16, 16-dimethyl prostaglandin E2 (dmPGE2) on gastric acid back diffusion and mucosal damage induced by 100 mg/kg of acidified tannic acid (tannic acid dissolved in 100 mm HCl + 54 mM NaCl solution) was studied in the vagotomized rat. Crude saikosaponin (500 mg/kg) given by intragastric irrigation (I.G.) produced a significant inhibition (p < 0.05), while dmPGE2 (100 micrograms/kg) provoked a significant increase (p < 0.05) in acid back diffusion induced by acid solution. When graded doses of SS (100-1000 mg/kg) were added to acidified tannic acid solution and instilled to the stomach, a dose-dependent inhibition in acidified tannic acid-induced mucosal ulceration and acid back diffusion was achieved. The decrease in the H+ concentration and the increase in the Na+ concentration in the final samples induced by acidified tannic acid were also significantly (p < 0.05) inhibited by the same doses of SS. However, neither intraduodenal (I.D.) nor intravenous (i.v.) administration of SS was effective in inhibiting these ulcerogenic parameters. When dmPGE2 (3-100 micrograms/kg) was given concomitantly with acidified tannic acid solution, the acid back diffusion as well as mucosal ulceration provoked by acidified tannic acid were not significantly improved. The volume of luminal contents but not electrolyte concentrations in the final sample was considerably increased by adding dmPGE2 to the acidified tannic acid solution. The failure of I.D. or i.v. of dmPGE2 in inhibiting tannic acid-induced acid back diffusion and mucosal ulceration was also observed in other series of experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

洪,C.R.,T.S. 吴和T.Y. 张。在迷走神经切断的大鼠中,研究了乙醇提取的柴胡皂苷(SS)和16,16 - 二甲基前列腺素E2(dmPGE2)对100 mg/kg酸化单宁酸(单宁酸溶解于100 mM HCl + 54 mM NaCl溶液)诱导的胃酸反向扩散和黏膜损伤的影响。经胃灌胃给予粗柴胡皂苷(500 mg/kg)产生了显著抑制作用(p < 0.05),而dmPGE2(100微克/千克)使酸溶液诱导的胃酸反向扩散显著增加(p < 0.05)。当将不同剂量的SS(100 - 1000 mg/kg)添加到酸化单宁酸溶液中并灌胃时,对酸化单宁酸诱导的黏膜溃疡和胃酸反向扩散实现了剂量依赖性抑制。相同剂量的SS也显著(p < 0.05)抑制了酸化单宁酸诱导的最终样本中H + 浓度的降低和Na + 浓度的升高。然而,十二指肠内(I.D.)或静脉内(i.v.)给予SS均不能有效抑制这些致溃疡参数。当dmPGE2(3 - 100微克/千克)与酸化单宁酸溶液同时给予时,酸化单宁酸引发的胃酸反向扩散以及黏膜溃疡并未得到显著改善。向酸化单宁酸溶液中添加dmPGE2可使最终样本中管腔内容物体积显著增加,但电解质浓度未改变。在其他系列实验中也观察到十二指肠内或静脉内给予dmPGE2不能抑制单宁酸诱导的胃酸反向扩散和黏膜溃疡。(摘要截短于250字)

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