Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Veterinary Medicine, China Agricultural University, Haidian, Beijing 100193, China.
Int J Mol Sci. 2019 Apr 4;20(7):1682. doi: 10.3390/ijms20071682.
Previous studies have demonstrated that monochromatic light affects plasma melatonin (MEL) levels, which in turn regulates hepatic insulin-like growth factor I (IGF-I) secretion via the Mel1c receptor. However, the intracellular signaling pathway initiated by Mel1c remains unclear. In this study, newly hatched broilers, including intact, sham operation, and pinealectomy groups, were exposed to either white (WL), red (RL), green (GL), or blue (BL) light for 14 days. Experiments in vivo showed that GL significantly promoted plasma MEL formation, which was accompanied by an increase in the MEL receptor, Mel1c, as well as phosphorylated extracellular regulated protein kinases (p-ERK1/2), and IGF-I expression in the liver, compared to the other light-treated groups. In contrast, this GL stimulation was attenuated by pinealectomy. Exogenous MEL elevated the hepatocellular IGF-I level, which is consistent with increases in cyclic adenosine monophosphate (cAMP), Gq, phosphorylated protein kinase C (p-PKC), and p-ERK1/2 expression. However, the Mel1c selective antagonist prazosin suppressed the MEL-induced expression of IGF-I, Gq, p-PKC, and p-ERK1/2, while the cAMP concentration was barely affected. In addition, pretreatment with Ym254890 (a Gq inhibitor), Go9863 (a PKC inhibitor), and PD98059 (an ERK1/2 inhibitor) markedly attenuated MEL-stimulated IGF-I expression and p-ERK1/2 activity. These results indicate that Mel1c mediates monochromatic GL-stimulated IGF-I synthesis through intracellular Gq/PKC/ERK signaling.
先前的研究表明，单色光会影响血浆褪黑素（MEL）水平，进而通过 Mel1c 受体调节肝脏胰岛素样生长因子 I（IGF-I）的分泌。然而，Mel1c 引发的细胞内信号通路仍不清楚。在这项研究中，新孵化的肉鸡包括完整组、假手术组和松果体切除术组，暴露于白光（WL）、红光（RL）、绿光（GL）或蓝光（BL）下 14 天。体内实验表明，与其他光照处理组相比，GL 显著促进了血浆 MEL 的形成，同时伴随着 MEL 受体 Mel1c 以及细胞外调节蛋白激酶（p-ERK1/2）和 IGF-I 在肝脏中的表达增加。相比之下，松果体切除术削弱了 GL 的这种刺激作用。外源性 MEL 提高了肝细胞 IGF-I 水平，与环腺苷酸（cAMP）、Gq、磷酸化蛋白激酶 C（p-PKC）和 p-ERK1/2 的表达增加一致。然而，Mel1c 选择性拮抗剂哌唑嗪抑制了 MEL 诱导的 IGF-I、Gq、p-PKC 和 p-ERK1/2 的表达，而 cAMP 浓度几乎没有受到影响。此外，Ym254890（Gq 抑制剂）、Go9863（PKC 抑制剂）和 PD98059（ERK1/2 抑制剂）的预处理显著减弱了 MEL 刺激的 IGF-I 表达和 p-ERK1/2 活性。这些结果表明，Mel1c 通过细胞内 Gq/PKC/ERK 信号转导介导单色 GL 刺激的 IGF-I 合成。
