山莨菪碱对志贺毒素1的保护作用:抑制细胞因子的产生,提高小鼠的存活率。

H. Zhang, Z. Ou, F. Gondaira, M. Ohmura, S. Kojio, T. Yamamoto
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引用次数: 17

摘要

本研究的目的是探讨山莨菪碱是否能抑制志贺毒素1 (Stx1)诱导的细胞因子的产生,并提高Stx1处理小鼠的存活率。Stx1 (1 ~ 100 ng/mL)加山莨菪碱(1 ~ 400 μ g/mL)刺激人单核细胞。在体内试验中,C57BL/6小鼠腹腔注射Stx1(2.75微克/千克)后,单次腹腔注射山莨菪碱(1毫克)或生理盐水。结果表明,山莨菪碱显著抑制stx1诱导的肿瘤坏死因子- α (tnf - α)、白细胞介素-1 β (il -1 β)和IL-8的产生。逆转录聚合酶链反应(RT-PCR)显示山莨菪碱抑制stx1介导的tnf - α mRNA表达。进一步的研究表明,这种抑制tnf - α的作用是通过前列腺素e2依赖的机制。山莨菪碱处理可延长小鼠存活时间,降低Stx1致死率(94.5% ~ 44%)。由于细胞因子,特别是tnf - α,参与了产stx大肠杆菌(STEC)感染的病理过程,本研究提示山莨菪碱可能是治疗STEC感染的潜在药物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Protective effect of anisodamine against Shiga toxin-1: inhibition of cytokine production and increase in the survival of mice.
The purpose of this study was to investigate whether anisodamine could inhibit Shiga toxin-1 (Stx1)-induced cytokine production and increase the survival of Stx1-treated mice. Human monocytic cells were stimulated by Stx1 (1 to 100 ng/mL) with or without anisodamine addition (1 to 400 microg/mL). For in vivo evaluations, C57BL/6 mice were given a single intraperitoneal injection of anisodamine (1 mg) or saline solution after intraperitoneal injection of Stx1 (2.75 microg/kg). The results showed that anisodamine significantly suppressed Stx1-induced tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and IL-8 production. Reverse transcriptase-polymerase chain reaction (RT-PCR) showed that anisodamine suppressed Stx1-mediated TNF-alpha mRNA expression. Further study showed that this TNF-alpha inhibitory effect was via a prostaglandin E2-dependent mechanism. Anisodamine treatment prolonged the survival time of mice and decreased the lethality of Stx1 (94.5% to 44%). Because cytokines, in particular TNF-alpha, contribute to the pathologic process in Stx-producing Escherichia coli (STEC) infection, this study suggested that anisodamine could be a potential drug for treatment of STEC infection.
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