| Title | beta(2)-adrenoceptor stimulation inhibits advanced glycation end products-induced adhesion molecule expression and cytokine production in human peripheral blood mononuclear cells. | | Author(s) | Takahashi HK, Mori S, Liu K, Wake H, Zhang J, Liu R, Yoshino T, Nishibori M | | Institution | Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama, Japan. | | Source | Eur J Pharmacol 2009 Oct 23. | | Abstract | 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 100mug/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. | | Language | ENG | | Pub Type(s) | JOURNAL ARTICLE
| | PubMed ID | 19857486 |
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