Phan Dieu-Hien, Shin Eun-Joo, Jeong Ji Hoon, Tran Hai-Quyen, Sharma Naveen, Nguyen Bao Trong, Jung Tae Woo, Nah Seung-Yeol, Saito Kuniaki, Nabeshima Toshitaka, Kim Hyoung-Chun
Neuropsychopharmacology and Toxicology Program, BK21 PLUS Project, College of Pharmacy, Kangwon National University, Chunchon, South Korea.
Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul, South Korea.
Clin Exp Pharmacol Physiol. 2020 May;47(5):790-797. doi: 10.1111/1440-1681.13243. Epub 2020 Jan 24.
In the present study, we investigated whether mood stabilizer lithium (Li) protects against d-amphetamine (AMP)-induced mania-like behaviours via modulating the novel proinflammatory potential. Repeated treatment with AMP resulted in significant increases in proinflammatory cyclooxygenase-2 (COX-2) and indolemaine-2,3-dioxygenase-1 (IDO)-1 expression in the prefrontal cortex (PFC) of mice. However, AMP treatment did not significantly change IDO-2 and 5-lipoxygenase (5-LOX) expression, suggesting that proinflammatory parameters such as COX-2 and IDO-1 are specific for AMP-induced behaviours. AMP-induced initial expression of COX-2 (15 minutes post-AMP) was earlier than that of IDO-1 (1 hour post-AMP). Mood stabilizer Li and COX-2 inhibitor meloxicam significantly attenuated COX-2 expression 15 minutes post-AMP, whereas IDO-1 inhibitor 1-methyl-DL-tryptophan (1-MT) did not affect COX-2 expression. However, AMP-induced IDO-1 expression was significantly attenuated by Li, meloxicam or 1-MT, suggesting that COX-2 is an upstream molecule for the induction of IDO-1 caused by AMP. Consistently, co-immunoprecipitation between COX-2 and IDO-1 was observed at 30 minutes, 1, 3, and 6 hours after the final AMP treatment. This interaction was also significantly inhibited by Li, meloxicam or 1-MT. Furthermore, AMP-induced hyperlocomotion was significantly attenuated by Li, meloxicam or 1-MT. We report, for the first time, that mood stabilizer Li attenuates AMP-induced mania-like behaviour via attenuation of interaction between COX-2 and IDO-1, and that the interaction of COX-2 and IDO-1 may be critical for the therapeutic intervention mediated by mood stabilizer.
在本研究中,我们调查了情绪稳定剂锂(Li)是否通过调节新发现的促炎潜能来预防右旋苯丙胺(AMP)诱导的躁狂样行为。用AMP重复处理导致小鼠前额叶皮质(PFC)中促炎环氧化酶-2(COX-2)和吲哚胺-2,3-双加氧酶-1(IDO)-1的表达显著增加。然而,AMP处理并未显著改变IDO-2和5-脂氧合酶(5-LOX)的表达,这表明诸如COX-2和IDO-1等促炎参数对AMP诱导的行为具有特异性。AMP诱导的COX-2初始表达(AMP给药后15分钟)早于IDO-1(AMP给药后1小时)。情绪稳定剂Li和COX-2抑制剂美洛昔康在AMP给药后15分钟显著减弱了COX-2的表达,而IDO-1抑制剂1-甲基-DL-色氨酸(1-MT)不影响COX-2的表达。然而,Li、美洛昔康或1-MT显著减弱了AMP诱导的IDO-1表达,这表明COX-2是AMP诱导IDO-1的上游分子。同样,在最后一次AMP处理后30分钟、1、3和6小时观察到COX-2和IDO-1之间的共免疫沉淀。Li、美洛昔康或1-MT也显著抑制了这种相互作用。此外,Li、美洛昔康或1-MT显著减弱了AMP诱导的运动亢进。我们首次报道,情绪稳定剂Li通过减弱COX-2和IDO-1之间的相互作用来减轻AMP诱导的躁狂样行为,并且COX-2和IDO-1的相互作用可能对情绪稳定剂介导的治疗干预至关重要。