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首页> 外文期刊>Life sciences >The antishock effect of anisodamine requires the upregulation of alpha7 nicotine acetylcholine receptors by IL-10.
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The antishock effect of anisodamine requires the upregulation of alpha7 nicotine acetylcholine receptors by IL-10.

机译：山iso碱的抗休克作用需要IL-10上调α7烟碱乙酰胆碱受体。

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AIMS: Although anisodamine, a muscarinic acetylcholine receptor antagonist, has been used in China for treating various shocks for many years, the mechanisms are not well understood. Our previous studies have demonstrated anisodamine exerts its cholinergic anti-inflammatory action through indirectly activating alpha7 nicotinic acetylcholine receptors (alpha7 nAChR). Because IL-10 is a critical anti-inflammatory factor, we investigated its potential role in the antishock action of anisodamine. MAIN METHODS: C57BL/6 and IL-10 -/- mice were intraperitoneally administered LPS and/or anisodamine, and the 24h survival rate, cytokine production and alpha7 nAChR expression were examined. In addition, RAW264.7 cells were stimulated with LPS, anisodamine and/or IL-10, and cytokine production and alpha7 nAChR expression were investigated. KEY FINDINGS: Anisodamine dose-dependently increased the 24h survival rate of C57BL/6 mice treated with LPS. The antishock role of anisodamine was significantly attenuated in IL-10 -/- mice. Anisodamine significantly decreased TNF-alpha and IL-1beta production in LPS-treated RAW264.7 cells and C57BL/6 mice. However, it did not increase the level of IL-10 in the same experiments. In RAW264.7 cells, IL-10 treatment increased alpha7 nAChR expression, which was further augmented in the presence of anisodamine. Spleens from IL-10 -/- mice expressed significantly lower alpha7 nAChRs levels compared to IL-10 +/+ mice. Although anisodamine markedly increased the expression of alpha7 nAChRs in spleens from LPS-treated IL-10 +/+ mice, it only induced a marginal increase of the receptor in spleens from LPS-treated IL-10 -/- mice. SIGNIFICANCE: These findings demonstrate that IL-10 plays an important role in the antishock action of anisodamine. It acts through upregulating alpha7 nAChR synergistically with anisodamine.
机译：目的：尽管山iso碱，一种毒蕈碱型乙酰胆碱受体拮抗剂，在中国已用于治疗多种电击已有多年历史，但其机理尚不十分清楚。我们以前的研究表明山iso碱通过间接激活α7烟碱乙酰胆碱受体（alpha7 nAChR）发挥其胆碱能抗炎作用。因为IL-10是关键的抗炎因子，所以我们研究了其在山iso碱的抗休克作用中的潜在作用。主要方法：腹膜内给予C57BL / 6和IL-10-/-小鼠LPS和/或山iso碱，并检查其24h存活率，细胞因子产生和alpha7 nAChR表达。此外，用LPS，山iso碱和/或IL-10刺激RAW264.7细胞，并研究了细胞因子的产生和alpha7 nAChR表达。主要发现：山iso碱剂量依赖性地提高了用LPS治疗的C57BL / 6小鼠的24小时生存率。在IL-10-/-小鼠中山iso胺的抗休克作用显着减弱。山iso碱显着降低LPS处理的RAW264.7细胞和C57BL / 6小鼠的TNF-α和IL-1beta产生。但是，在相同的实验中，它并没有增加IL-10的水平。在RAW264.7细胞中，IL-10处理可增加alpha7 nAChR表达，并在山amine碱存在下进一步增强。与IL-10 + / +小鼠相比，IL-10-/-小鼠的脾脏表达的α7nAChRs水平明显降低。尽管山iso碱明显增加了LPS处理的IL-10 + / +小鼠脾脏中α7nAChRs的表达，但仅诱导了LPS治疗的IL-10-/-小鼠脾脏中受体的少量增加。意义：这些发现表明IL-10在山iso碱的抗休克作用中起重要作用。它通过与山iso碱协同上调alpha7 nAChR发挥作用。

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