Protective effects of melatonin against ethanol-induced reactive gliosis in hippocampus and cortex of young and aged rats
Protective effects of melatonin against ethanol-induced reactive gliosis in hippocampus and cortex of young and aged rats
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DOI：
10.1016/j.expneurol.2005.02.003
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发表时间：
2005-07-01
影响因子：
5.3
通讯作者：
Tuzcu, M
中科院分区：
文献类型：
--
作者：
Baydas, G;Tuzcu, M
越来越多的证据表明，长期摄入乙醇会导致中枢神经系统细胞活力的直接或间接变化。研究了衰老和长期乙醇消耗对大鼠胶质标记物[胶质纤维酸性蛋白（GFAP）和S100B]以及氧化和抗氧化状态的影响。此外，还分析了褪黑激素对衰老和饮酒的保护作用。年轻和老年大鼠长期服用乙醇会导致脂质过氧化增加，谷胱甘肽 (GSH) 水平下降，而同时服用褪黑激素可显着逆转这一现象。与年轻大鼠相比，接受酒精治疗的老年大鼠的脂质过氧化状态受到显着影响。在皮质和海马体中发现 GFAP 和 S100B 水平与年龄相关。长期饮酒导致幼龄大鼠GFAP含量明显升高（P < 0.01），而老年大鼠皮质含量升高幅度较小（P < 0.05）。在老年大鼠中，酒精处理没有显着改变海马 GFAP 水平（P > 0.05）。褪黑素与酒精共同给药显着降低了老年大鼠海马（P < 0.01）和皮质（P < 0.001）中的 GFAP 含量。没有发现酒精治疗对老年大鼠神经元特异性烯醇化酶（NSE）水平有显着影响。这一发现表明，褪黑激素通过清除自由基和稳定神经胶质细胞活性来对抗乙醇和衰老的破坏作用，从而对受损的神经组织发挥保护作用。此外，这项工作表明，启动神经胶质细胞增生的信号是由自由基形成介导的，至少是间接介导的。 (c) 2005 Elsevier Inc. 保留所有权利。
Evidence has been accumulated indicating that chronic ethanol consumption leads to direct or indirect changes in the viability of central nervous system cells. The effects of aging and chronic ethanol consumption on glial markers [glial fibrillary acidic protein (GFAP) and S100B] and oxidant and antioxidant status of rats were studied. Furthermore, protective effects of melatonin against aging and alcohol consumption were also assayed. Chronic ethanol administration to young and aged rats produced an increase in lipid peroxidation, and a decline in glutathione (GSH) levels, which was significantly reversed by the co-administration of melatonin. Lipid peroxidation status was markedly affected in aged rats treated with alcohol compared to the young rats. An age-related increase in GFAP and S100B levels were found in the cortex and hippocampus. Long-term alcohol exposure resulted in distinct elevation in GFAP content in young rats (P < 0.01) while there was less increase in the cortex of aged rats (P < 0.05). In old rats, hippocampat GFAP levels were not significantly changed by alcohol treatment (P > 0.05). Co-administration of melatonin with alcohol significantly reduced GFAP contents both in the hippocampus (P < 0.01) and cortex (P < 0.001) of aged rats. No significant effects of alcohol treatment were found on the levels of neuron-specific enolase (NSE) in aged rats. This finding suggests that melatonin exerts its protective effect on injured nervous tissues by scavenging free radicals and stabilizing glial activity against the damaging effects of ethanol and aging. Furthermore, this work suggests that the signal to initiate gliosis is mediated, at least indirectly, by free radical formation. (c) 2005 Elsevier Inc. All rights reserved.