Curcumin treatment attenuates alcohol-induced alterations in a mouse model of foetal alcohol spectrum disorders

被引:24
作者
Cantacorps, Lidia [1 ]
Montagud-Romero, Sandra [1 ]
Valverde, Olga [1 ,2 ]
机构
[1] Univ Pompeu Fabra, Dept Expt & Hlth Sci, Neurobiol Behav Res Grp GReNeC NeuroBio, Parc Recerca Biomed Barcelona,C Dr Aiguader 88, Barcelona 08003, Spain
[2] IMIM Hosp del Mar, Res Inst, Neurosci Res Programme, Barcelona, Spain
关键词
Foetal alcohol spectrum disorders; Curcumin; Alcohol; Behaviour; Neuroinflammation; Epigenetics; NF-KAPPA-B; ADENOSINE A(2A) RECEPTORS; PRENATAL ETHANOL EXPOSURE; NITRIC-OXIDE SYNTHASE; COGNITIVE IMPAIRMENTS; EPIGENETIC CHANGES; MEMORY DEFICITS; NEUROINFLAMMATION; ACTIVATION; RATS;
D O I
10.1016/j.pnpbp.2020.109899
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Alcohol exposure during development produces physical and mental abnormalities in the foetus that result in long-term molecular adjustments in the brain, which could underlie the neurobehavioural deficits observed in individuals suffering from foetal alcohol spectrum disorders. In this study, we assessed the effects of curcumin on cognitive impairments caused by prenatal and lactational alcohol exposure (PLAE). Furthermore, we examined whether curcumin could counteract the molecular alterations that may underlie these behavioural impairments. We focused on inflammatory and epigenetic mechanisms by analysing the expression of pro-inflammatory mediators, such as IL-6, TNF-alpha, and NF-kappa B, in the hippocampus and prefrontal cortex, as well as microglia and astrocyte activation in the dentate gyrus. We also assessed the activity of histone acetyltransferase in these brain areas. To model binge alcohol drinking, we exposed pregnant C57BL/6 mice to a 20% v/v alcohol solution during gestation and lactation, with limited access periods. We treated male offspring with curcumin during postnatal days (PD28-35) and then evaluated their behaviour in adulthood (PD60). Our results showed that curcumin treatment during the peri-adolescence period improved the anxiety and memory deficits observed in PLAE mice. At the molecular level, we found enhanced histone acetyltransferase activity in mice subjected to PLAE that curcumin treatment could not reverse to baseline levels. These mice also showed increased expression of pro-inflammatory mediators, which could be rescued by curcumin treatment. They also displayed astrogliosis and microglia activation. Our study provides further evidence to support the use of curcumin as a therapeutic agent for counteracting behavioural and molecular alterations induced by PLAE.
引用
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页数:11
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