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消炎痛对肠炎沙门氏菌、大肠杆菌和霍乱弧菌不耐热肠毒素介导的皮肤通透性反应的抑制作用。

Inhibitory effect of indomethacin on skin permeability reactions mediated by heat-labile enterotoxins of Salmonella weltevreden, Escherichia coli and Vibrio cholerae.

作者信息

Kaura Y K, Sharma V K

出版信息

Zentralbl Bakteriol Mikrobiol Hyg A Med Mikrobiol Infekt Parasitol. 1982 May;252(1):35-42.

PMID:6750983
Abstract

Indomethacin, a rapid and intense inhibitor of prostaglandin synthesis, was used with a view to find out similarity in secretory mechanism of heat-labile enterotoxins of three diarrhoea producing enteric bacteria viz., Salmonella weltevreden, Escherichia coli and Vibrio cholerae in rabbits. A significant inhibition (90% to 94%) of biological activity of indomethacin pretreated Salmonella enterotoxin was evident in indomethacin treated rabbits, whereas the biological activity was found comparatively low (28% to 76%) in the untreated enterotoxin preparations. In contrast, the skin permeability reaction to cholera toxin remained unaltered in the absence of pretreatment of cholera toxin with indomethacin and it dropped to 55% in pre-treated toxin preparations. There was complete inhibition of biological activity of E. coli enterotoxin which did not receive indomethacin pretreatment. Based on these observations it may be inferred that indomethacin inhibits skin permeability response of heat labile enterotoxin of S. weltevreden both by blocking the effect of prostaglandins (Blocking mechanism) as well as by prostaglandin-adenyl cyclase pathway. The reduction in the biological activity of cholera toxin seems to be occurring through blocking of prostaglandins by indomethacin. In case of E. coli enterotoxin the inhibition mechanism seems operating through prostaglandin-adenyl cyclase system. These observations indicate that the Salmonella enterotoxin shares some similarity with enterotoxins of E. coli and Vibrio cholerae in respect of mechanism of action.

摘要

消炎痛是一种快速且强效的前列腺素合成抑制剂,使用它的目的是探究三种致腹泻肠道细菌,即肠炎沙门氏菌、大肠杆菌和霍乱弧菌的不耐热肠毒素在兔子体内分泌机制的相似性。在消炎痛处理过的兔子中,经消炎痛预处理的肠炎沙门氏菌肠毒素的生物活性有显著抑制(90%至94%),而在未经处理的肠毒素制剂中,生物活性相对较低(28%至76%)。相比之下,在霍乱毒素未用消炎痛预处理的情况下,其皮肤通透性反应保持不变,而在预处理的毒素制剂中,该反应降至55%。未接受消炎痛预处理的大肠杆菌肠毒素的生物活性被完全抑制。基于这些观察结果可以推断,消炎痛通过阻断前列腺素的作用(阻断机制)以及前列腺素 - 腺苷酸环化酶途径来抑制肠炎沙门氏菌不耐热肠毒素的皮肤通透性反应。霍乱毒素生物活性的降低似乎是通过消炎痛阻断前列腺素而发生的。对于大肠杆菌肠毒素,抑制机制似乎是通过前列腺素 - 腺苷酸环化酶系统起作用。这些观察结果表明,肠炎沙门氏菌肠毒素在作用机制方面与大肠杆菌和霍乱弧菌的肠毒素有一些相似之处。

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