壳寡糖对乙醇诱导的炎症反应的保护作用

Protective Effect of Chitosan Oligosaccharide on Ethanol Induced Inflammatory Reaction

为研究壳寡糖对酒精损伤海马组织的保护作用,将39只新生SD大鼠随机分为3组,分别是空白对照组(CON组)、模型组(ETOH组)和壳寡糖干预组(COS组)。建立新生SD大鼠酒精损伤模型,对COS组进行壳寡糖干预,在出生后第9天(PD9)干预结束,在PD9到PD24之间不再进行干预,分别检测PD9和PD24的磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(Akt)、胶质纤维酸性蛋白(GFAP)和凋亡诱导因子(AIF1)的表达,炎症因子白细胞介素6(IL-6)、白细胞介素10(IL-10)、肿瘤坏死因子α(TNF-α)的表达量,在PD24进行新物体识别试验。结果表明:在PD9时,COS组中PI3K和Akt及其磷酸化水平、GFAP和AIF1蛋白水平与ETOH组相比无显著差异,IL-10显著增加,IL-6和TNF-α显著降低。在PD24时,与ETOH组相比,COS组中PI3K、Akt蛋白的磷酸化水平显著上升,GFAP表达下降,IL-10显著增加,IL-6和TNF-α显著降低。壳寡糖可以在PD24缓解PI3K/Akt通路的抑制,抑制星形胶质细胞标志物GFAP的过表达,在PD9和PD24抑制IL-6和TNF-α的过表达,缓解IL-10的抑制。

To study the protective effect of chitosan oligosaccharide on alcohol-induced hippocampal tissue,39 newborn SD rats were randomly divided into three groups:Blank control group(CON group),model group(ETOH group)and chitosan oligosaccharide intervention group(COS group).The alcohol injury model of newborn SD rats was established.The COS group received chitosan oligosaccharide intervention.At the end of the intervention on the 9th day after birth(PD9),no intervention was conducted between PD9 and PD24.The phosphatidylinositol-4,5-bisphosphoinositol-3-kinase(PI3K)/protein kinase B(Akt)of PD9 and PD24 were observed respectively expression of glial fibrillary acidic protein(GFAP)and apoptosis-inducing factor1(AIF1),inflammatory factors interleukin 6(IL-6),interleukin 10(IL-10),tumor necrosis factorα(tumor necrosis factor alpha,TNF-α).The new object recognition experiment is carried out at PD24.The results showed that at PD9,PI3K,Akt proteins and their phosphorylation levels,GFAP and AIF1 protein in COS group were not significantly different from those in ETOH group,but IL-6 and IL-10 were significantly increased,TNF-αsignificantly decreased.At PD24,compared with ETOH group,the phosphorylation level of PI3K and Akt protein in COS group increased significantly,the expression of GFAP decreased,IL-6 and IL-10 increased significantly,and TNF-αsignificantly decreased.Chitosan oligosaccharide can alleviate the inhibition of PI3K/Akt pathway and inhibit the overexpression of astrocyte marker GFAP in PD24.