Melatonin

Melatonin is a hormone made by the pineal gland that can activates melatonin receptor. Melatonin plays a role in sleep and possesses important antioxidative and anti-inflammatory properties[1][2][3]. Melatonin is a novel selective ATF-6 inhibitor and induces human hepatoma cell apoptosis through COX-2 downregulation[4].

Melatonin increases the levels of activated PTEN, RSK-1, mTOR and AMPKα kinases, mildly inhibits ERK-1/2 phosphorylation and Bad phosphorylation, significantly inhibits phosphorylations of S6 Ribosomal Protein, 4E-BP1, GSK-3α and GSK-3β, and slightly increases PRAS40 phosphorylation in animals[1]. Melatonin ameliorates the neurotoxiciy and astrocyte activation induced by Aβ1-42 in the cerebral cortex. Melatonin also blocks the reduction in Reelin and Dab1 expression induced by Aβ1-42[2]. Melatonin treatment and lack of NLRP3-/- share similar inhibition of NF-κB and NLRP3 signaling pathway in mice. Melatonin treatment and lack of NLRP3-/- share some patterns of clock genes expression, and improve cardiomyocytes morphology in mice[3].

References:
[1]. Kilic U, et al. Particular phosphorylation of PI3K/Akt on Thr308 via PDK-1 and PTEN mediates melatonin's neuroprotective activity after focal cerebral ischemia in mice. Redox Biol. 2017 Apr 5;12:657-665
[2]. Hu C, et al. Neuroprotective effect of melatonin on soluble Aβ1-42-induced cortical neurodegeneration via Reelin-Dab1 signaling pathway. Neurol Res. 2017 Apr 7:1-1
[3]. Rahim I, et al. Melatonin administration to wild-type mice and non-treated NLRP3 mutant mice share similar inhibition of the inflammatory response during sepsis. J Pineal Res. 2017 Mar 31
[4]. Bu LJ, et al. Melatonin, a novel selective ATF-6 inhibitor, induces human hepatoma cell apoptosis through COX-2 downregulation. World J Gastroenterol. 2017 Feb 14;23(6):986-998.

褪黑激素是由松果体产生的一种激素，可以激活褪黑激素受体。褪黑素在睡眠中发挥作用，具有重要的抗氧化和抗炎特性[1][2][3]。褪黑素是一种新型选择性ATF-6抑制剂，通过下调COX-2诱导人肝癌细胞凋亡[4]。

褪黑素可增加动物体内活化的PTEN、RSK-1、mTOR和AMPKα激酶的水平，轻度抑制ERK-1/2磷酸化和Bad磷酸化，显著抑制S6核糖体蛋白、4E-BP1、GSK-3α和GSK-3β的磷酸化，并轻微增加PRAS40磷酸化[1]。褪黑素可改善Aβ1-42在大脑皮层诱导的神经毒性和星形胶质细胞活化。褪黑素还阻断Aβ1-42诱导的Reelin和Dab1表达的减少[2]。褪黑素治疗和缺乏NLRP3-/-对小鼠NF-κB和NLRP3信号通路的抑制作用相似。褪黑素治疗和缺乏NLRP3-/-共享一些时钟基因表达模式，并改善小鼠心肌细胞形态[3]。