title: NE strengthens the immunosuppression induced by AlCl₃ through β₂-AR/cAMP pathway in cultured rat peritoneal macrophages.
abstract: To investigate the effect of noradrenaline (NE) on the immunosuppression induced by aluminum trichloride (AlCl3), the peritoneal macrophages were cultured with RPMI-1640 medium containing 0.97 mM AlCl3 (1/10 IC50). NE was added to the medium at the final concentrations of 0 (control group, N-C), 0.1 (low-dose group, N-L), 1 (mid-dose group, N-M), and 10 (high-dose group, N-H) nM, respectively. No addition of both AlCl3 and NE serviced as blank group (D-C). Chemotaxis, adhesion, phagocytosis, tumor necrosis factor α (TNF-α) secretion, cyclic adenosine monophosphate (cAMP) content, β2 adrenergic receptors (β2-AR) density, and messenger RNA (mRNA) expression of macrophages were detected. The results showed that AlCl3 reduced the chemotaxis, adhesion, phagocytosis, and TNF-α secretion and increased the cAMP content, β2-AR density, and mRNA expression of peritoneal macrophages. Meanwhile, the chemotaxis, adhesion, phagocytosis, TNF-α secretion, β2-AR density, and mRNA expression were reduced while the cAMP content was increased in NE-treated groups than those in N-C group. The results indicated that NE strengthens the immunosuppression induced by AlCl3 in cultured rat peritoneal macrophages through the β2-AR/cAMP pathway.
authors.affiliation: College of Veterinary Medicine, Northeast Agricultural University, 150030, Harbin, China.
authors.forename: Miao
authors.initials: M
authors.lastname: Li
authors.forename: Xu
authors.initials: X
authors.lastname: Yang
authors.forename: Cuicui
authors.initials: C
authors.lastname: Zhuang
authors.forename: Zheng
authors.initials: Z
authors.lastname: Cao
authors.forename: Limin
authors.initials: L
authors.lastname: Ren
authors.forename: Chunyu
authors.initials: C
authors.lastname: Xiu
authors.forename: Yanfei
authors.initials: Y
authors.lastname: Li
authors.forename: Yanzhu
authors.initials: Y
authors.lastname: Zhu
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000077410:Aluminum Chloride; D017607:Aluminum Compounds / Q000494:pharmacology*; D000818:Animals; D002478:Cells, Cultured; D002633:Chemotaxis / Q000187:drug effects / Q000276:immunology; D002712:Chlorides / Q000494:pharmacology*; D000242:Cyclic AMP / Q000276:immunology* / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D015870:Gene Expression / Q000187:drug effects / Q000276:immunology; D007108:Immune Tolerance / Q000187:drug effects*; D017737:Macrophages, Peritoneal / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D009638:Norepinephrine / Q000494:pharmacology*; D010587:Phagocytosis / Q000187:drug effects / Q000276:immunology; D017208:Rats, Wistar; D018343:Receptors, Adrenergic, beta-2 / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000187:drug effects / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology / Q000378:metabolism
chemical_list: D000316:Adrenergic alpha-Agonists; D017607:Aluminum Compounds; D002712:Chlorides; D018343:Receptors, Adrenergic, beta-2; D014409:Tumor Necrosis Factor-alpha; D000077410:Aluminum Chloride; D000242:Cyclic AMP; D009638:Norepinephrine