壳聚糖复方制剂对脂肪肝大鼠的治疗作用及其机制的探讨

目的 :进一步研究壳聚糖复方制剂对实验性脂肪肝大鼠的治疗作用及其机制。方法 :采用小剂量CCl4 致肝损伤并高脂饮食建立大鼠脂肪肝模型 ,给予模型大鼠壳聚糖复方制剂 0 .7g·kg- 1·d- 1灌服 8wk ,检测肝脏三酰甘油 (TG )、总胆固醇(TC)、血清及肝脏游离脂肪酸 (FFA)含量 ,检测肝脂变面积及肝脏过氧化物酶体增殖物激活受体α(PPARα)mRNA的表达情况。结果 :CCl4 损伤并高脂饮食可引起实验性大鼠肝脏明显脂肪变性 ,肝脏TG ,TC ,FFA及血清FFA含量升高 ,肝细胞PPARαmRNA表达减少。与模型组比较 ,壳聚糖复方制剂能明显降低肝脏TG ,TC ,FFA及血清FFA含量(P <0 .0 1) ,提高肝细胞PPARαmRNA的表达(P <0 .0 1)。结论 :壳聚糖复方制剂对实验性脂肪肝大鼠具有一定的治疗作用 ,其作用机制可能与其诱导PPARα表达 ,促进肝脏摄取、氧化脂肪酸有关。

Therapeutic effect and mechanisms of chitosan compound on rats of experimental fatty liver

AIM: To further study the therapeutic effect of chitosan compound on rats of experimental fatty liver and it's mechanisms. METHODS: Male SD rats were treated with a small dosage of CCl 4 and fed by a high-lipid diet for 6 wk to induce fatty liver model. Then the therapeutic group was ig chitosan compound with 0.7g·kg -1·d -1 for 8 wk. The steatosis degree was determined by the contents of lipids in the rat liver, and the free fatty acid(FFA) of blood and liver, the expression of peroxisome proliferator activated receptor α(PPARα) were measured. RESULTS: Combined use of CCl 4 and high-lipid diet increased significantly the contents of triglyceride(TG), total cholesterol(TC) and FFA in liver or in serum and markedly decrease the expression of the PPARα mRNA. Compared with the model group, the chitosan compound could obviously decrease the contents of TG, TC, FFA in liver and FFA in serum, and increase the PPARα mRNA expression, respectively(P<0.01). CONCLUTION: The results indicate that chitosan compound is effective in treating rat fatty liver by inducing PPARα mRNA expression and promoing liver intake and oxidation of fatty acid.