Pharmacology Research Laboratory, University Institute of Pharmaceutical Sciences, UGC Center of Advanced Study, Panjab University, Chandigarh 160014, India.
Psychopharmacology (Berl). 2012 Dec;224(4):519-35. doi: 10.1007/s00213-012-2779-9. Epub 2012 Jul 13.
Clinical and experimental evidence have demonstrated that alcohol consumption during pregnancy can disrupt brain development, leading to a variety of behavioral alterations including hyperactivity, motor dysfunction, and cognitive deficits in offsprings. Alcohol-induced neurocognitive deficits are associated with activation of oxidative-inflammatory cascade coupled with extensive apoptotic neurodegeneration in different brain regions.
The present study was designed with an aim to investigate the protective effect of curcumin, a principal curcuminoid present in the Indian spice turmeric, against alcohol-induced cognitive deficits, neuroinflammation, and neuronal apoptosis in rat pups postnatally exposed to ethanol.
Male Wistar rat pups were administered ethanol (5 g/kg, 12 % v/v) by intragastric intubation on postnatal days (PD) 7, 8, and 9 and were treated with curcumin (30 and 60 mg/kg) from PD 6 to 28. Performance of ethanol-exposed pups that did not receive curcumin was significantly impaired as evaluated in both Morris water maze and elevated plus maze tasks recorded by using computer tracking. Cognitive deficit was associated with enhanced acetylcholinesterase activity, increased neuroinflammation (oxidative-nitrosative stress, TNF-α, IL-1β, and TGF-β1), and neuronal apoptosis (NF-κβ and caspase 3) in both cerebral cortex and hippocampus of ethanol-exposed pups. Chronic treatment with curcumin significantly ameliorated all the behavioral, biochemical, and molecular alterations in different brain regions of ethanol-exposed pups.
The current study demonstrates the possible involvement of oxidative-inflammatory cascade-mediated apoptotic signaling in cognitive deficits associated with postnatal ethanol exposure and points towards the neuroprotective potential of curcumin in mitigating alcohol-induced behavioral, biochemical, and molecular deficits.
临床和实验证据表明，怀孕期间饮酒会破坏大脑发育，导致后代出现各种行为改变，包括多动、运动功能障碍和认知缺陷。酒精引起的神经认知缺陷与氧化炎症级联的激活以及不同大脑区域广泛的凋亡性神经退行性变有关。
本研究旨在探讨姜黄素（印度香料 turmeric 中的主要姜黄素类化合物）对大鼠幼仔出生后暴露于乙醇的认知缺陷、神经炎症和神经元凋亡的保护作用。
雄性 Wistar 幼鼠在出生后第 7、8 和 9 天通过胃内灌胃给予乙醇（5g/kg，12%v/v），并从第 6 天到第 28 天给予姜黄素（30 和 60mg/kg）。未给予姜黄素的乙醇暴露幼鼠的表现明显受损，这是通过计算机跟踪在 Morris 水迷宫和高架十字迷宫任务中评估得出的。认知缺陷与乙酰胆碱酯酶活性增强、神经炎症（氧化-硝化应激、TNF-α、IL-1β 和 TGF-β1）以及神经元凋亡（NF-κβ 和 caspase 3）有关，这些都发生在乙醇暴露幼鼠的大脑皮质和海马体中。姜黄素的慢性治疗显著改善了乙醇暴露幼鼠不同大脑区域的所有行为、生化和分子改变。
本研究表明，氧化炎症级联介导的凋亡信号可能参与了与出生后乙醇暴露相关的认知缺陷，并指出了姜黄素在减轻酒精引起的行为、生化和分子缺陷方面的神经保护潜力。
