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Effect of melatonin on monochromatic light-induced T-lymphocyte proliferation in the thymus of chickens

松果体切除术 褪黑素 氯吲哚 内分泌学 内科学 敌手 生物 刀豆蛋白A 褪黑激素受体 淋巴细胞 受体 松果体 分子生物学 体外 医学 生物化学
作者
Fuju Chen,Aikebaier Reheman,Jing Cao,Zixu Wang,Yulan Dong,Yu-Xian Zhang,Yaoxing Chen
出处
期刊:Journal of Photochemistry and Photobiology B-biology [Elsevier BV]
卷期号:161: 9-16 被引量:42
标识
DOI:10.1016/j.jphotobiol.2016.05.001
摘要

A total of 360 post-hatching day 0 (P0) Arbor Acre male broilers, including intact, sham operation and pinealectomy groups, were exposed to white light (WL), red light (RL), green light (GL) and blue light (BL) from a light-emitting diode (LED) system until for P14. We studied the effects of melatonin and its receptors on monochromatic light-induced T-lymphocyte proliferation in the thymus of broilers. The density of proliferating cell nuclear antigen (PCNA) cells and the proliferation of T-lymphocytes in response to Concanavalin A (ConA) in GL significantly increased both in vivo and in vitro (from 9.57% to 32.03% and from 34.30% to 50.53%, respectively) compared with other lights (p<0.005) and was strongly correlated with melatonin levels in plasma (p<0.005). Pinealectomy reduced the levels of circulatory melatonin and the proliferation of T-lymphocytes and eliminated the differences between GL and other lights (p<0.005). However, exogenous melatonin (10(-9)M) significantly increased the proliferative activity of T-lymphocyte by 9.64% (p=0.002). In addition, GL significantly increased mRNA expression levels of Mel1a, Mel1b and Mel1c receptors from 21.09% to 32.57%, and protein expression levels from 24.43% to 42.92% compared with RL (p<0.05). However, these effects were blocked after pinealectomy. Furthermore, 4P-PDOT (a selective Mel1b antagonist) and prazosin (a selective Mel1c antagonist) attenuated GL-induced T-lymphocyte proliferation in response to ConA (p=0.000). Luzindole (a nonselective Mel1a/Mel1b antagonist), however, did not induce these effects (p=0.334). These results suggest that melatonin may mediate GL-induced T-lymphocyte proliferation via the Mel1b and Mel1c receptors but not via the Mel1a receptor.
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