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目的通过蛋氨酸-胆碱缺乏(Methionine-Choline-Deficient,MCD)饮食诱导的小鼠脂肪性肝炎(NonAlcoholic Steatohepatitis,NASH)模型研究虾青素抗非酒精性脂肪肝纤维化效应及其机制。方法将30只雄性C57BL/6J小鼠随机分为对照组、模型组和虾青素组,每组10只。模型组饲喂MCD饲料,对照组在MCD饲料基础上每kg饲料添加3 g L-蛋氨酸和2 g胆碱;虾青素组在MCD饲料基础上用虾青素口服液灌胃(20 mg/kg.bw),每周2次。4周后,称量各组小鼠体重、肝重并计算肝脏指数;测定小鼠血清TG、TC、ALT、AST及肝脏TG、TC水平。肝组织苏木素和伊红(Hematoxylin and Eosin,HE)染色观察组织形态学变化;荧光定量PCR检测α-平滑肌肌动蛋白(α-Smooth Muscle Actin,α-SMA)和Ⅰ型胶原的m RNA表达水平。结果模型组小鼠血清ALT、AST水平,肝脏TG、TC水平及α-SMA和Ⅰ型胶原的m RNA表达与对照组相比显著升高(P<0.05),上述指标虾青素组与模型组相比显著降低(P<0.05);模型组和虾青素组小鼠血清TG、TC水平与对照组相比显著降低(P<0.05)。HE染色结果表明,模型组肝组织可见大量脂肪变性,而虾青素组脂肪变性程度明显减轻。结论虾青素可以改善肝功能,且可能通过调控α-SMA和Ⅰ型胶原基因的表达减缓MCD饮食诱导的非酒精性脂肪肝纤维化进程。
Objective To investigate the effects of astaxanthin on nonalcoholic fatty liver fibrosis induced by Methionine-Choline-Deficient (MCD) diet in mice and its mechanism. Methods Thirty male C57BL / 6J mice were randomly divided into control group, model group and astaxanthin group, with 10 rats in each group. The model group was fed with MCD diet, and the control group was fed with 3 g L-methionine and 2 g choline per kg feed on the basis of MCD diet. The astaxanthin group was fed with astaxanthin oral solution (20 mg / kg.bw) twice a week. Four weeks later, the body weight and liver weight of each group were weighed, and the liver index was calculated. The levels of TG, TC, ALT, AST in serum and TG and TC in liver were measured. Hematoxylin and eosin (HE) staining of liver tissue was used to observe the histomorphological changes. The mRNA expression level of α-smooth muscle actin (α-SMA) and collagen Ⅰ was detected by real-time PCR. . Results The levels of serum ALT, AST, hepatic TG, TC and the mRNA expressions of α-SMA and collagen type Ⅰ in model group were significantly higher than those in control group (P <0.05). The astaxanthin group and model (P <0.05). The levels of serum TG and TC in model group and astaxanthin group were significantly lower than those in control group (P <0.05). The results of HE staining showed that a large amount of steatosis was observed in liver tissue of the model group while the degree of steatosis was significantly reduced in the astaxanthin group. Conclusion Astaxanthin can improve liver function, and may reduce the non-alcoholic fatty liver fibrosis induced by MCD diet by regulating the expression of α-SMA and type Ⅰ collagen.