Aluko Oritoke M, Umukoro Solomon
Department of Physiology, School of Health and Health Technology, Federal University of Technology, Akure, Nigeria.
Neuropharmacology Unit, Department of Pharmacology and Therapeutics, Faculty of Basic Medical Sciences, University of Ibadan, Ibadan, Nigeria.
Naunyn Schmiedebergs Arch Pharmacol. 2020 Dec;393(12):2339-2353. doi: 10.1007/s00210-020-01939-6. Epub 2020 Jul 14.
Unpredictable chronic mild stress (UCMS) has been shown to cause memory loss via increased oxidative stress and deregulation of monoaminergic and cholinergic neurotransmissions. Although the benefits of methyl jasmonate (MJ), a well-known anti-stress plant hormone against chronic stress-induced psychopathologies, have been earlier reported, its effects on antioxidant defense molecules, monoaminergic transmitters, and nuclear factor erythroid 2-related factor 2 (Nrf2) immunopositive cells have not been extensively studied. The present study was designed to examine its effect on memory functions, antioxidant biomarkers, monoaminergic transmitters, and Nrf2 immunopositive cell expression in rats exposed to UCMS. Rats received an intraperitoneal injection of MJ (10, 25, and 50 mg/kg) 30 min before exposure to UCMS daily for 28 days. Memory function was assessed on day 29 using a modified elevated plus maze and novel object recognition tests. The antioxidant biomarkers, level of monoamines (serotonin, noradrenaline, and dopamine), and Nrf2 immunopositive cell expression were determined in the rat brain tissues. The activity of cholinesterase and monoamine oxidase enzymes was also determined. MJ attenuated memory deficits and elevated the brain levels of monoamines in UCMS rats. UCMS-induced increase of brain cholinesterase and monoamine oxidase activities was inhibited by MJ. Also, MJ attenuated UCMS-induced decrease in antioxidant enzymes (CAT, GPx, GST, and SOD) and thiol contents in the brains of rats. UCMS-induced increase in NO level and Nrf2 immunopositive cell expression in the rat's brain was attenuated by MJ. Taken together, these findings suggest that increasing antioxidant defense molecules and monoaminergic/cholinergic neurotransmitters and decreasing the Nrf2 immunopositive cell expressions may contribute to the memory-promoting effects of MJ in rats exposed to UCMS.
不可预测的慢性轻度应激（UCMS）已被证明可通过增加氧化应激以及单胺能和胆碱能神经传递失调导致记忆丧失。尽管茉莉酸甲酯（MJ）作为一种著名的抗应激植物激素，其对慢性应激诱导的精神病理学有益作用已有早期报道，但其对抗氧化防御分子、单胺能递质和核因子红细胞2相关因子2（Nrf2）免疫阳性细胞的影响尚未得到广泛研究。本研究旨在检测其对暴露于UCMS的大鼠记忆功能、抗氧化生物标志物、单胺能递质和Nrf2免疫阳性细胞表达的影响。大鼠在每天暴露于UCMS前30分钟腹腔注射MJ（10、25和50毫克/千克），持续28天。在第29天使用改良的高架十字迷宫和新物体识别测试评估记忆功能。测定大鼠脑组织中的抗氧化生物标志物、单胺（血清素、去甲肾上腺素和多巴胺）水平以及Nrf2免疫阳性细胞表达。还测定了胆碱酯酶和单胺氧化酶的活性。MJ减轻了UCMS大鼠的记忆缺陷并提高了大脑中的单胺水平。MJ抑制了UCMS诱导的大脑胆碱酯酶和单胺氧化酶活性增加。此外，MJ减轻了UCMS诱导的大鼠脑中抗氧化酶（CAT、GPx、GST和SOD）和硫醇含量的降低。MJ减弱了UCMS诱导大鼠脑中NO水平升高和Nrf2免疫阳性细胞表达增加。综上所述，这些发现表明增加抗氧化防御分子和单胺能/胆碱能神经递质以及减少Nrf2免疫阳性细胞表达可能有助于MJ对暴露于UCMS大鼠的记忆促进作用。
