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首页> 外文期刊>European Journal of Pharmacology: An International Journal >Beta2-adrenoceptor stimulation inhibits advanced glycation end products-induced adhesion molecule expression and cytokine production in human peripheral blood mononuclear cells.
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Beta2-adrenoceptor stimulation inhibits advanced glycation end products-induced adhesion molecule expression and cytokine production in human peripheral blood mononuclear cells.

机译:Beta 2肾上腺素能受体刺激抑制人类外周血单核细胞中晚期糖基化终产物诱导的粘附分子表达和细胞因子产生。

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Cell-to-cell interaction through binding of intercellular adhesion molecule-1 (ICAM-1) and CD40 on monocytes to their ligands on T-cells plays crucial roles in cytokine production. Advanced glycation end products (AGEs) subtypes induce complications in diabetes. In a previous study, we found that glyceraldehyde-derived AGE (AGE-2) and glycolaldehyde-derived AGE (AGE-3) at 100 microg/ml induced the expressions of ICAM-1 and CD40 on monocytes and the production of interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha in human peripheral blood mononuclear cells. beta(2)-adrenoceptor stimulation has been demonstrated to modulate the production of inflammatory mediators. In the present study, we found that norepinephrine, epinephrine and isoproterenol inhibited AGE-2- and AGE-3-induced adhesion expression and cytokine production in a concentration-dependent manner. The action of these catecholamines was antagonized by beta(2)-adrenoceptor antagonist, but not by alpha(1)-, alpha(2)- and beta(1)-adrenoceptor antagonist. beta(2)-adrenoceptor agonists, salbutanol and terbutaline inhibited AGE-2- and AGE-3-induced adhesion expression and cytokine production, but alpha(1)-, alpha(2)- and beta(1)-adrenoceptor agonist had no effect, indicating that the stimulation of beta(2)-adrenoceptor might improve AGEs-initiated complications in diabetes.
机译:通过单核细胞上的细胞间粘附分子-1(ICAM-1)和CD40结合至T细胞上的配体的细胞间相互作用在细胞因子产生中起着至关重要的作用。晚期糖基化终产物(AGEs)亚型可诱发糖尿病并发症。在先前的研究中,我们发现100微克/毫升的甘油醛衍生的AGE(AGE-2)和乙醇醛衍生的AGE(AGE-3)诱导单核细胞上ICAM-1和CD40的表达以及干扰素(IFN)的产生。 -γ和人类外周血单核细胞中的肿瘤坏死因子(TNF)-α。 β(2)-肾上腺素受体刺激已被证明可以调节炎症介质的产生。在本研究中,我们发现去甲肾上腺素,肾上腺素和异丙肾上腺素以浓度依赖的方式抑制AGE-2-和AGE-3诱导的黏附表达和细胞因子的产生。这些儿茶酚胺的作用被β(2)-肾上腺素受体拮抗剂拮抗,但不受α(1)-,α(2)-和β(1)-肾上腺素受体拮抗剂拮抗。 β(2)-肾上腺素受体激动剂,沙丁胺醇和特布他林抑制AGE-2-和AGE-3诱导的粘附表达和细胞因子产生,但alpha(1)-,α(2)-和beta(1)-肾上腺素受体激动剂没有效果,表明刺激β(2)-肾上腺素受体可能会改善AGEs引发的糖尿病并发症。

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