D-柠檬烯对大鼠酒精性肝损伤脂质代谢紊乱的影响

发布时间：2018-01-23 08:21

本文关键词： D-柠檬烯酒精性肝损伤脂质代谢紊乱谷丙转氨酶谷草转氨酶甘油三酯总胆固醇低密度脂蛋白胆固醇　出处：《食品科学》2015年05期 　论文类型：期刊论文

【摘要】：探讨D-柠檬烯(D-limonene)对大鼠酒精性肝损伤脂质代谢紊乱的保护作用及可能作用机制,利用持续酒精灌胃的方法建立大鼠酒精肝损伤模型,分为A、B、C、D、E、F、G共7组。A组为空白对照组,每日给予蒸馏水灌胃,前2周8 m L/(kg·d),后4周12 m L/(kg·d);B组为酒精模型组,每日灌胃体积分数为50%的乙醇,前2周8 m L/(kg·d),后4周12 m L/(kg·d);C、D、E组分别为D-柠檬烯低、中、高剂量组,每日分别灌胃D-柠檬烯100、200、400 m L/(kg·d),其中D-柠檬烯与A、B组等量的50%的乙醇混合后灌胃;F组为水和D-柠檬烯空白高剂量组,每日给予D-柠檬烯400 m L/(kg·d);G组为甘利欣药物对照组,灌胃量200 m L/(kg·d)。HE染色和电镜观察肝组织形态结构和肝组织超微结构的变化,测定血清谷丙转氨酶(alanine transaminase,ALT)、谷草转氨酶(aspartate transaminase,AST)、碱性磷酸酶(phosoporic acid,ALP)、胆碱酯酶(cholinesterase,CHE)、甘油三酯(triglyceride,TG)、胆固醇(cholesterol,CHO)、低密度脂蛋白胆固醇(low density lipoprotein-cholesterol,LDL-C)水平。结果电镜下观察到A组肝细胞结构正常,核呈圆形或椭圆,线粒体形态正常。B组肝细胞次级溶酶体数量增加,线粒体形状不规则,脂滴多。C组可见少量脂滴,高尔基体正常,线粒体清楚。D组少量脂滴,胆小管有内容物,线粒体正常。E组线粒体高尔基体正常,少量脂滴,核圆。F组细胞器无异常,少量脂滴。G组少量脂滴,偶见溶酶,体线粒体正常。B组大鼠血清ALT、AST、ALP、CHE、TG、CHO、LDL-C均高于空白对照组,差异显著(P0.05);F组大鼠血清所测各指标与空白对照组无明显差异;而D-柠檬烯低、中、高剂量干预组和酒精模型组比较,血清所测各指标水平均有不同程度地降低,其中D-柠檬烯中、高剂量干预组血清所测各指标水平明显低于酒精模型组,差异显著(P0.05)。结论:过量酒精摄入引起的肝组织超微结构病理损伤与升高血清ALP、CHE、ALT、AST、TG、CHO、LDL-C水平,在D-柠檬烯干预下有所减轻和降低。因此,D-柠檬烯可调节过量酒精摄入造成的脂质代谢紊乱。
[Abstract]:To investigate the protective effect of D-limonene (D-limonene) on lipid metabolism disorder in rats with alcoholic liver injury and its possible mechanism, a rat model of alcoholic liver injury was established by continuous alcohol administration. Group A was divided into 7 groups: group A was treated with distilled water daily (8 mL / kg 路d). After 4 weeks, 12 mL / kg / d; Group B was treated with alcohol model group, the volume fraction of ethanol was 50% per day, 8 mL / kg / d for the first 2 weeks and 12 mL / kg / d for the last 4 weeks. The low, middle and high doses of Dlimonene were given intragastrically to Dlimonene 100,200,400 mL / kg 路dl / d group respectively, among which D- limonene and A. In group B, 50%% ethanol was mixed into the stomach; Group F was treated with water and high dose of D-limonene blank, and was given Dlimonene 400 mL / L / kg / d daily. Group G was treated with glycyrrhizin as control group. The changes of liver morphology and ultrastructure were observed by HE staining and electron microscopy. Serum alanine transaminase (alt) and aspartate transaminase (AST) were measured. Alkaline phosphatase, cholinesterase, triglyceride. TGG, cholesterol cholesterol Cho. Low density lipoprotein cholesterol density lipoprotein-cholesterol. Results the structure of hepatocytes in group A was normal, the nucleus was round or ellipse, and the number of secondary lysosomes of hepatocytes in group B was increased and the shape of mitochondria was irregular. A small amount of lipid droplets were found in group C with normal Golgi apparatus, a small amount of lipid droplets were found in group D with clear mitochondria, and there were contents in bile tubules. In group E, the Golgi body of mitochondria was normal and a small amount of lipid drops were found in group E. There was no abnormal organelle in the nuclear circle group, a few lipid drops in the group G, and occasionally lysozyme, and the serum ALTASTASTERCHEN TGG Cho was found in the normal mitochondria of the rats in group B (P < 0.05). LDL-C was significantly higher than that of control group (P 0.05). There was no significant difference in serum indexes between group F and control group. Compared with the alcohol model group, the serum levels of each index of D- limonene were decreased to some extent, especially in D- limonene. The serum levels of the high dose intervention group were significantly lower than that of the alcohol model group (P 0.05). Conclusion: the ultrastructural pathological damage of liver tissue induced by excessive alcohol intake and the increase of serum ALP in the high dose intervention group were significantly lower than those in the alcohol model group. The level of LDL-C in TGG was reduced and decreased with the intervention of D- limonene. D-limonene can regulate lipid metabolism disorder caused by excessive alcohol intake.
【作者单位】：青岛大学医学院医学营养研究所;
【基金】：“十二五”国家科技支撑计划项目(2012BAD33B01) 国家自然科学基金面上项目(31171671)
【分类号】：R151
【正文快照】： 近几十年以来,酒精滥用一直是全球性的公共健康问题[1]。长期过量饮酒可引发酒精性肝病(alcoholic liverdisease,ALD),ALD是一种进行性疾病,早期病理改变为肝细胞氧化损伤,进一步可发展为酒精性脂肪肝,发展到晚期则无法治愈,因此在肝细胞氧化损伤之前干预有重要意义[2-6]。从

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