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首页> 外文期刊>Cellular Physiology and Biochemistry >Chronic β-adrenoceptor antagonists upregulate the rat alveolar macrophage adrenergic system through the β~1-subtype
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Chronic β-adrenoceptor antagonists upregulate the rat alveolar macrophage adrenergic system through the β~1-subtype

机译：慢性β-肾上腺素受体拮抗剂通过β〜1-亚型上调大鼠肺泡巨噬细胞肾上腺素系统

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Previous studies demonstrate that macrophages synthesis and release catecholamines, which regulate the immune responses in an autocrine manner. These responses are mediated in part by β-adrenoceptors expressed on macrophages. Some β-adrenoceptor antagonists are commonly used in clinical conditions. Here we investigated whether the chronic administration of β-adrenoceptor antagonists upregulate adrenergic system of alveolar macrophage and the potential mechanims. Methods: Propranolol (30 mg/kg·d) or atenolol (5 mg/kg·d) was administered by gavage to rats for 4 weeks. Then alveolar macrophages were isolated and the expression of β_1 or β_2-adrenoceptor was detected by flow cytometric analysis. Dopamine β-hydroxylase expression was assessed by Western blot assay and the concentrations of noradrenaline, IL-6, and TNF-α in cell supernatants were measured using ELISA after 2 h or 24 h exposure of alveolar macrophages to 100 ng/ml lipopolysaccharide (LPS). Results: Propranolol increased the mean fluorescence intensity (MFI) of β_1, β_2- adrenoceptor and the frequency of β_1-,β_2- adrenoceptor positive macrophages. However, only the MFI of β_1- adrenoceptor and the frequency of β_1-adrenoceptor positive macrophages were increased by atenolol. Furthermore, both propranolol and atenolol promoted LPS-mediated dopamine β-hydroxylase protein expression and increased noradrenaline production in rat alveolar macrophages. This was accompanied by increased LPS-mediated IL-6 and TNF-α production in cell supernatants of alveolar macrophages. Conclusion: These findings demonstrate that propranolol or atenolol upregulates alveolar macrophage adrenergic system, and the response may be β_1-adrenergic receptor subtype dependent.
机译：先前的研究表明巨噬细胞合成并释放儿茶酚胺，后者以自分泌方式调节免疫反应。这些反应部分地由在巨噬细胞上表达的β-肾上腺素受体介导。一些β-肾上腺素受体拮抗剂通常用于临床状况。在这里，我们调查了长期服用β-肾上腺素能受体拮抗剂是否会上调肺泡巨噬细胞的肾上腺素能系统和潜在的机制。方法：强饲法对大鼠普萘洛尔30 mg / kg·d或阿替洛尔5 mg / kg·d 4周。然后分离肺泡巨噬细胞，并通过流式细胞术检测β_1或β_2-肾上腺素受体的表达。肺泡巨噬细胞暴露于100 ng / ml脂多糖（LPS）2 h或24 h后，通过ELISA测定多巴胺β-羟化酶的表达，并用ELISA测定细胞上清液中去甲肾上腺素，IL-6和TNF-α的浓度）。结果：普萘洛尔提高了β_1，β_2-肾上腺素受体的平均荧光强度（MFI）和β_1，β_2-肾上腺素受体阳性巨噬细胞的频率。然而，阿替洛尔仅增加了β_1-肾上腺素受体的MFI和β_1-肾上腺素受体阳性巨噬细胞的频率。此外，普萘洛尔和阿替洛尔均促进大鼠肺泡巨噬细胞中LPS介导的多巴胺β-羟化酶蛋白表达并增加去甲肾上腺素的生成。这伴随着肺泡巨噬细胞细胞上清液中LPS介导的IL-6和TNF-α产生的增加。结论：这些发现表明普萘洛尔或阿替洛尔上调了肺泡巨噬细胞的肾上腺素能系统，其反应可能是β_1-肾上腺素能受体亚型的依赖。

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