Korkmaz H, Temel T, Bugdaci M S, Tekelioglu Y, Ozoran Y, Kapicioglu S
Bratisl Lek Listy. 2014;115(4):185-9. doi: 10.4149/bll_2014_039.
We aimed to investigate the effect of fish oil on the hepatic injury and cell cycle phases as well as cellular proliferation- regeneration in a rat model of acute hepatic injury induced by carbon tetrachloride.
Compensatory cell proliferation and tissue regeneration occurs as an endogenous response following chemical damage to the liver and enable animals to over come the injury. Data related to effect of fish oil on liver injury induced by chemical hepatotoxicants are controversial.
60 male Wistar-albino rats were fed either with a diet supplemented with 20% fish oil or standard rat feed for 2 weeks. After an overnight fast, rats in each group were administered either 1 ml/kg carbon tetrachloride or saline intraperitoneally.
Fish oil enriched diet significantly enhanced the carbon tetrachloride - associated necroinflammatory damage, ballooning degeneration and the elevation of serum transaminases induced by carbon tetrachloride. Furthermore fish oil diet prevented cell proliferation, increased the proportion of cells in the G0/G1phase concomitant with a decrease in the proportion of cells in the S phase cells.
Fish oil diet exacerbates the hepatic injury and prevents cell proliferation-regeneration in normal and injured liver cells. Suppression of tissue regeneration by fish oil may lead to progression of the hepatic injury (Tab. 3, Fig. 4, Ref. 31).
我们旨在研究鱼油对四氯化碳诱导的急性肝损伤大鼠模型中肝损伤、细胞周期阶段以及细胞增殖-再生的影响。
代偿性细胞增殖和组织再生是肝脏受到化学损伤后的内源性反应，使动物能够克服损伤。关于鱼油对化学性肝毒物诱导的肝损伤影响的数据存在争议。
60只雄性Wistar白化大鼠分别喂食添加20%鱼油的饲料或标准大鼠饲料，持续2周。禁食过夜后，每组大鼠腹腔注射1 ml/kg四氯化碳或生理盐水。
富含鱼油的饮食显著增强了四氯化碳相关的坏死性炎症损伤、气球样变性以及四氯化碳诱导的血清转氨酶升高。此外，鱼油饮食抑制了细胞增殖，增加了G0/G1期细胞的比例，同时S期细胞的比例降低。
鱼油饮食会加重肝损伤，并抑制正常和受损肝细胞的增殖-再生。鱼油对组织再生的抑制可能导致肝损伤的进展（表3，图4，参考文献31）。
