Effect of Chitooligosaccharide on Ethanol-Induced Oxidative Stress Injury and Apoptotic Factors in Neonatal Rat Brain

被引:0
|
作者
Wang B. [1 ,2 ]
Chen Y. [1 ,2 ]
Xia W. [1 ,2 ]
机构
[1] School of Food Science and Technology, Jiangnan University, Wuxi
[2] Collaborative Innovation Center of Food Safety and Quality Control in Jiangsu Province, Wuxi
来源
Shipin Kexue/Food Science | 2022年 / 43卷 / 07期
关键词
Apoptosis; Chitooligosaccharide; Ethanol-induced brain damage; Oxidative stress;
D O I
10.7506/spkx1002-6630-20210313-173
中图分类号
学科分类号
摘要
The purpose of this study was to investigate the protective effect of chitooligosaccharide (COS) against alcoholinduced 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. © 2022, China Food Publishing Company. All right reserved.
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页码:105 / 111
页数:6
相关论文
共 29 条
  • [1] MOORE E S, WARD R E, JAMISON P L, Et al., The subtle facial signs of prenatal exposure to alcohol: an anthropometric approach, The Journal of Pediatrics, 139, 2, pp. 215-219, (2001)
  • [2] WILHOIT L F, SCOTT D A, SIMECKA B A., Fetal alcohol spectrum disorders: characteristics, complications, and treatment, Community Mental Health Journal, 53, 6, pp. 711-718, (2017)
  • [3] GRANATO A, DERING B., Alcohol and the developing brain: Why neurons die and how survivors change, International Journal of Molecular Sciences, 19, 10, (2018)
  • [4] NASH K, SHEARD E, ROVET J, Et al., Understanding fetal alcohol spectrum disorders (FASDs): toward identification of a behavioral phenotype, Scientific World Journal, 8, 3, pp. 873-882, (2008)
  • [5] WILLOUGHBY K A, SHEARD E D, NASH K, Et al., Effects of prenatal alcohol exposure on hippocampal volume, verbal learning, and verbal and spatial recall in late childhood, Journal of the International Neuropsychological Society, 14, 6, pp. 1022-1033, (2008)
  • [6] KOMADA M, HARA N, KAWACHI S, Et al., Mechanisms underlying neuro-inflammation and neurodevelopmental toxicity in the mouse neocortex following prenatal exposure to ethanol, Scientific Reports, 7, 1, (2017)
  • [7] SCHREIBER W B, ST CYR S A, JABLONSKI S A, Et al., Effects of exercise and environmental complexity on deficits in trace and contextual fear conditioning produced by neonatal alcohol exposure in rats, Developmental Psychobiology, 55, 5, pp. 483-495, (2013)
  • [8] MURAWSKI N J, STANTON M E., Effects of dose and period of neonatal alcohol exposure on the context preexposure facilitation effect, Alcoholism Clinical and Experimental Research, 35, 6, pp. 1160-1170, (2011)
  • [9] OLNEY J W, ISHIMARU M J, BITTIGAU P, Et al., Ethanol-induced apoptotic neurodegeneration in the developing brain, Apoptosis, 5, 6, pp. 515-521, (2000)
  • [10] OLNEY J W, TENKOVA T, DIKRANIAN K, Et al., Ethanol-induced caspase-3 activation in the in vivo developing mouse brain, Neurobiology of Disease, 9, 2, pp. 205-219, (2002)