Kurihara T, Adachi Y, Yamagata M, Abe K, Akimoto M, Hashimoto H, Ishiguro H, Niimi A, Maeda A, Shigemoto M
Department of Gastroenterology, Aoyama Hospital, Tokyo Women's Medical College, Japan.
Clin Ther. 1994 Sep-Oct;16(5):830-7.
Choline-deficient feed was given to three groups (n = 7 in each) of male Sprague-Dawley rats for 4 weeks to induce the development of fatty liver. In addition, two of the groups received eicosapentaenoic acid (EPA), 1000 mg/kg/d, administered orally either for all 4 weeks or for only the last 2 weeks of the study, respectively. The third group received the choline-deficient diet but no EPA. The untreated control group (n = 7) received only normal feed. The efficacy of EPA in preventing fatty liver was assessed based on the evaluation of pathologic and biochemical parameters and hepatic blood flow. EPA markedly improved fatty liver, probably due to both direct effects (inhibition of the synthesis of triglyceride in the liver) and indirect effects (increased hepatic blood flow). Decreased blood flow due to sinusoidal block is responsible for the progression of fatty liver. EPA has been shown to decrease thromboxane A2 production and blood viscosity and to enhance red cell deformability. These effects are thought to have contributed to the increases in hepatic blood flow.
给三组雄性斯普拉格-道利大鼠（每组n = 7）喂食胆碱缺乏饲料4周，以诱导脂肪肝的形成。此外，其中两组分别在整个4周或仅在研究的最后2周口服二十碳五烯酸（EPA），剂量为1000 mg/kg/天。第三组接受胆碱缺乏饮食但不补充EPA。未处理的对照组（n = 7）仅喂食正常饲料。基于病理和生化参数以及肝血流评估了EPA预防脂肪肝的功效。EPA显著改善了脂肪肝，这可能归因于直接作用（抑制肝脏中甘油三酯的合成）和间接作用（增加肝血流）。由于肝血窦阻塞导致的血流减少是脂肪肝进展的原因。已表明EPA可减少血栓素A2的产生和血液粘度，并增强红细胞变形能力。这些作用被认为有助于增加肝血流。
