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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Chronic propranolol treatment affects expression of adrenoceptors on peritoneal macrophages and their ability to produce hydrogen peroxide and nitric oxide.
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Chronic propranolol treatment affects expression of adrenoceptors on peritoneal macrophages and their ability to produce hydrogen peroxide and nitric oxide.

机译:慢性普萘洛尔治疗影响腹膜巨噬细胞上肾上腺素受体的表达及其产生过氧化氢和一氧化氮的能力。

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Using both immunocytochemical and flow cytometric analyses of rat peritoneal exudate cells constitutive expression of tyrosine hydroxylase and both beta(2)- and alpha(1)- adrenoceptors on macrophages was revealed. Furthermore, according to the characteristic assemblage of tyrosine hydroxylase and adrenoceptor subtype expression different macrophage subsets were identified. In vitro treatment of macrophages with the non-selective alpha,beta-adrenoceptor agonist arterenol and/or the beta-adrenoceptor antagonist propranolol indicated that beta-adrenoceptors potentiated nitric oxide (NO) production and suggested alpha-adrenoceptor-mediated suppression of hydrogen peroxide (H(2)O(2)) production. An increase in H(2)O(2) production in the presence of the alpha(1)-adrenoceptor antagonist ebrantil provided support for this. Chronic propranolol treatment in vivo led to increased NO and H(2)O(2) production by peritoneal macrophages. Furthermore, this treatment resulted in opposing effects on the expression of beta(2)- and alpha(1)-adrenoceptors on peritoneal macrophages (a stimulatory effect on beta(2)-adrenoceptors and a suppressive effect on alpha(1)-adrenoceptors). In conclusion, a subset of resident peritoneal macrophages synthesizes catecholamines, which may exert differential effects on H(2)O(2) and NO production via distinct adrenoceptors. Finally, chronic propranolol treatment affected adrenoceptor expression on peritoneal macrophages and altered their capacity to generate NO and H(2)O(2).
机译:使用免疫细胞化学和流式细胞仪分析大鼠腹膜渗出液细胞的酪氨酸羟化酶和巨噬细胞上的β(2)-和α(1)-肾上腺素受体的组成型表达被揭示。此外,根据酪氨酸羟化酶和肾上腺素受体亚型表达的特征组合,鉴定了不同的巨噬细胞亚群。用非选择性α,β-肾上腺素受体激动剂和/或β-肾上腺素受体拮抗剂普萘洛尔对巨噬细胞进行体外治疗表明,β-肾上腺素能增强一氧化氮(NO)的产生,并建议由α-肾上腺素受体介导的过氧化氢抑制( H(2)O(2))生产。在存在alpha(1)-肾上腺素能受体拮抗剂ebrantil的情况下增加H(2)O(2)的生产为此提供了支持。体内的慢性普萘洛尔治疗导致腹膜巨噬细胞的NO和H(2)O(2)生产增加。此外,这种治疗对腹膜巨噬细胞的beta(2)-和alpha(1)-肾上腺素受体的表达产生相反的影响(对beta(2)-肾上腺素受体的刺激作用和对alpha(1)-肾上腺素受体的抑制作用) 。总之,驻留腹膜巨噬细胞的一个子集合成儿茶酚胺,可能通过不同的肾上腺素受体对H(2)O(2)和NO产生不同的影响。最后,慢性普萘洛尔治疗影响腹膜巨噬细胞上肾上腺素受体的表达,并改变其生成NO和H(2)O(2)的能力。

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