| 赵娜 徐会 王赫 王钧毅 齐社宁 杨俊涛.小蘖碱抑制游离脂肪酸诱导小鼠肝实质细胞脂肪变性[J].现代生物医学进展英文版,2015,15(1):14-17. |
| 小蘖碱抑制游离脂肪酸诱导小鼠肝实质细胞脂肪变性 |
| Berberine Inhibits the Steatosis of Parenchymal Hepacyto Induced by FFAs |
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| DOI： |
| 中文关键词: 小蘖碱 游离脂肪酸 肝实质细胞 脂肪变性 |
| 英文关键词: Berberine FFAs Hepatocyte Steatosis |
| 基金项目:重大科学仪器研究专项（2013YQ140405）；国家自然科学基金青年学者基金项目（31000405）；
国家高技术研究发展计划(2012AA020201)；科技重大专项（2013ZX10002009-001） |
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| 中文摘要: |
| 目的：探讨小蘖碱（Berberine）对游离脂肪酸（free fatty acids，FFAs）诱导的小鼠肝实质细胞脂肪变性的影响。方法：胶原酶灌
注分离BALB/c 小鼠原代肝实质细胞并体外培养。分对照组，高脂组，高脂加小蘖碱处理组。体外测定细胞内甘油三酯的含量。利
用油红染色观察细胞的脂肪样变性。通过Western印迹法检测肝实质细胞内MAPK相关信号通路磷酸化的变化。实时定量PCR
检测肝实质细胞中与脂肪化密切相关的miR-122 的表达和相关靶基因的表达改变。结果：与高脂组比较，小蘖碱处理组肝实质细
胞内甘油三酯含量降低，脂肪颗粒减少，脂肪变性明显改善，并具有明显的剂量效应，小蘖碱能够抑制FFAs 诱导的JNK 通路磷
酸化。Q-PCR 结果表明小蘖碱能够促进肝实质细胞内miR-122 的表达，并降低脂肪化相关基因Dgat2 的表达。结论：小蘖碱能够
显著改善高脂诱发的肝脂肪变性，抑制JNK通路磷酸化，其机制可能同miR-122 通路相关。 |
| 英文摘要: |
| Objective:To research the influence of Berberine on liver steatosis induced by free fatty acids（free fatty acids, FFAs）
fromliver parenchymal cells.Methods:Mouse primary hepatocytes were isolated by a two-step collegenase perfusion procedure and cultured
in vitro. Cells were divided into three groups, the control group, FFAs group and FFAs plus berberine treatment group. The content
of triglyceride was determined in vitro. Steatosis was analyzed by oil red O staining. The MAPK related signal pathway was analyzed by
Western-blot assay. Real-time PCR was used to detect the expression of miR-122 which was closely related to fat and relevant target
genes in liver parenchymal cells.Results:Compared with FFAs group, berberine treatment decreased the content of triglyceride and fat
particles significantly and improved steatosis obviously in liver parenchymal cells in a dose-dependent manner. Berberine could effectively
inhibit phosphorylation of JNK pathway induced by FFAs. Q-PCR results showed that berberine could up-regulate the expression of
miR-122 while down-regulate the expression of Dgat2.Conclusion:Berberine can significantly improve the steatosis induced by FFAs
and inhibit phosphorylation of JNK pathway by a possible mechanismof miR-122 pathway. |
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