School of Nutrition and Health Sciences, Taipei Medical University, Taipei 110, Taiwan.
Research Center of Geriatric Nutrition, College of Nutrition, Taipei Medical University, Taipei 110, Taiwan.
Mediators Inflamm. 2017;2017:5801768. doi: 10.1155/2017/5801768. Epub 2017 Dec 13.
Sixty male Wistar rats were fed a control or an ethanol-containing diet in groups C or E. The fat compositions were adjusted with 25% or 57% fish oil substituted for olive oil in groups CF25, CF57, EF25, and EF57. Hepatic thiobarbituric acid-reactive substance (TBARS) levels, cytochrome P450 2E1 protein expression, and tumor necrosis factor- (TNF-) , interleukin- (IL-) 1, IL-6, and IL-10 levels, as well as intracellular adhesion molecule (ICAM)-1 levels were significantly elevated, whereas plasma adiponectin level was significantly reduced in group E ( < 0.05). Hepatic histopathological scores of fatty change and inflammation, in group E were significantly higher than those of group C ( < 0.05). Hepatic TBARS, plasma ICAM-1, and hepatic TNF-, IL-1, and IL-10 levels were significantly lower, and plasma adiponectin levels were significantly higher in groups EF25 and EF57 than those in group E ( < 0.05). The immunoreactive area of the intestinal tight junction protein, ZO-1, showed no change between groups C and E. Only group CF57 displayed a significantly higher ZO-1 immunoreactive area compared to group C ( = 0.0415). 25% or 57% fish oil substituted for dietary olive oil could prevent ethanol-induced liver damage in rats, but the mechanism might not be related to intestinal tight junction ZO-1 expression.
60 只雄性 Wistar 大鼠分别被喂食对照或含乙醇饮食,分为 C 或 E 组。CF25、CF57、EF25 和 EF57 组用 25%或 57%的鱼油替代橄榄油调整脂肪组成。E 组的肝丙二醛(TBARS)水平、细胞色素 P450 2E1 蛋白表达、肿瘤坏死因子-(TNF-)、白细胞介素-(IL-)1、IL-6 和 IL-10 水平以及细胞间黏附分子(ICAM)-1 水平显著升高,而血浆脂联素水平显著降低(<0.05)。E 组的肝脂肪变性和炎症组织学评分明显高于 C 组(<0.05)。EF25 和 EF57 组的肝 TBARS、血浆 ICAM-1 以及肝 TNF-、IL-1 和 IL-10 水平显著低于 E 组,而血浆脂联素水平显著高于 E 组(<0.05)。C 和 E 组之间肠道紧密连接蛋白 ZO-1 的免疫反应面积没有变化。仅 CF57 组与 C 组相比,ZO-1 免疫反应面积显著增加(=0.0415)。用 25%或 57%的鱼油替代饮食中的橄榄油可以预防乙醇诱导的大鼠肝损伤,但机制可能与肠道紧密连接 ZO-1 表达无关。