| 引用本文: | 那日苏,张海峰.维生素C通过调节PPAR-α靶基因抑制高脂饮食诱导非酒精性脂肪肝小鼠[J].中国现代应用药学,2021,38(22):2791-2795. |
| NA Risu,ZHANG Haifeng.Vitamin C Inhibits the Nonalcoholic Fatty Liver Induced by High Fat Diet in Mice Regulating PPAR-α Target Gene[J].Chin J Mod Appl Pharm(中国现代应用药学),2021,38(22):2791-2795. |
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| 摘要: |
| 目的 探讨维生素C是否通过调节PPAR-α靶基因抑制高脂饮食诱导非酒精性脂肪肝（nonalcoholic fatty liver disease，NAFLD）小鼠模型。方法 C57BL/6小鼠随机分为对照组、NAFLD组和维生素C组。每组均为10只小鼠。对照组采用普通饲料连续喂养15周；NAFLD组采用高脂饲料连续喂养15周；维生素C组采用高脂饲料及维生素C连续喂养15周。喂养15周后，利用代谢测量、组织学和基因表达检查NAFLD相关因素。结果 与NAFLD组小鼠相比，补充维生素C可抑制NAFLD小鼠体质量增加（P<0.05）。同时，维生素C组小鼠循环维生素C浓度显著高于NAFLD组（P<0.05）。维生素C可抑制肝脏脂肪变性（P<0.05）。同样，维生素C也可使NAFLD小鼠肝脏炎症、纤维化和凋亡相关基因mRNA水平降低（均P<0.05）。此外，维生素C小鼠血清丙氨酸转氨酶、天冬氨酸转氨酶、总胆固醇和低密度脂蛋白胆固醇水平低于NAFLD小鼠（均P<0.05）。最后，维生素C还能提高肝脏PPAR-α介导脂肪酸β氧化基因mRNA水平（均P<0.05）。结论 维生素C对NAFLD小鼠体质量增加、肝脏甘油三酯积累，以及肝脏炎症、纤维化和凋亡有抑制作用，这一过程可能部分是通过上调PPAR-α靶基因表达介导的。 |
| 关键词: 维生素C 非酒精性脂肪肝 小鼠 |
| DOI：10.13748/j.cnki.issn1007-7693.2021.22.005 |
| 分类号:R965.1 |
| 基金项目:内蒙古自治区自然科学基金项目（2020MS08108）；内蒙古自治区卫生计生科研计划项目（201701046）；内蒙古医科大学科技百万工程项目（YKD2016KJBW018） |
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| Vitamin C Inhibits the Nonalcoholic Fatty Liver Induced by High Fat Diet in Mice Regulating PPAR-α Target Gene |
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NA Risu1, ZHANG Haifeng2
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1.Inner Mongolia Medical University, Department of Pathophysiology, Hohhot 010110, China;2.Inner Mongolia Medical University, Department of Physiology, Hohhot 010110, China
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| Abstract: |
| OBJECTIVE To explore whether vitamin C could inhibit high-fat diet induced nonalcoholic fatty liver disease (NAFLD) mouse model by regulating PPAR-α target gene. METHODS C57BL/6 mice were divided into control group, NAFLD group and vitamin C group. Each group consisted of 10 mice. The control group was fed with normal diet for 15 weeks; the NAFLD group was fed with high-fat diet for 15 weeks; vitamin C group were fed with high-fat diet and vitamin C for 15 weeks. After 15 weeks of feeding, variables and determinants of NAFLD were examined using metabolic measurements, histology, and gene expression. RESULTS Compared to NAFLD group mice, administration of vitamin C to obese mice reduced body weight gain(P<0.05). Concomitantly, circulating vitamin C concentrations were significantly higher in vitamin C mice than in NAFLD mice(P<0.05). Vitamin C could inhibit hepatic steatosis(P<0.05). Similarly, vitamin C also reduced the mRNA levels of liver inflammation, fibrosis and apoptosis related genes in NAFLD mice(all P<0.05). In addition, serum alanine aminotransferase, aspartate aminotransferase, total cholesterol and low density lipoproteincholesterol levels in vitamin C mice were lower than those in NAFLD mice(all P<0.05). Vitamin C could also increase the mRNA level of PPAR-α-mediated fatty acid β oxidation gene in liver(all P<0.05). CONCLUSION Vitamin C can inhibit weight gain, liver triglyceride accumulation, liver inflammation, fibrosis and apoptosis in NAFLD mice, which may be partly mediated by up regulating PPAR-α target gene expression. |
| Key words: vitamin C nonalcoholic fatty liver mice |
