关键词: 壳寡糖；酒精诱导脑损伤；氧化应激；凋亡

Abstract: The purpose of this study was to investigate the protective effect of chitooligosaccharide (COS) against alcohol-induced oxidative stress injury and neuronal cell apoptosis in the brain of neonatal rats. In total, 56 neonatal SD rats were randomly divided into four groups: normal control (NC), COS, model (MOD), and COS + MOD. The effect of COS on body mass change, histopathology, oxidative stress injury and the expression of apoptosis-associated proteins was evaluated. The results showed that oral administration of alcohol slowed down body mass gain and caused necrosis and deformation of brain nerve cells, but this effect was relieved by intervention with COS. Additionally, intervention with COS increased the levels of superoxide dismutase (SOD) activity, glutathione (GSH) content and total antioxidant capacity (T-AOC), and significantly reduced malondiadehyde (MDA) level in brain tissue. COS significantly relieved oxidative stress damage caused by ethanol exposure in the brain of neonatal rats, and reduced the expression of cleaved caspase-3. These results indicated that COS protects against brain damage induced by ethanol in neonatal rats, and the underlying mechanism may be related to the fact that COS can alieve ethanol-induced oxidative stress injury of brain tissue and inhibit neuronal cell apoptosis.

Key words: chitooligosaccharide; ethanol-induced brain damage; oxidative stress; apoptosis