芹菜素对肥胖型小鼠脂肪组织AMPK信号通路的作用机制

黄链莎; 刘铜华; 孙文; 郭璇; 李迎真; 陈淑惠; 周鹏

doi:10.13422/j.cnki.syfjx.20180816

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芹菜素对肥胖型小鼠脂肪组织AMPK信号通路的作用机制

中药干预糖尿病研究专题 | 更新时间：2024-01-04

- 芹菜素对肥胖型小鼠脂肪组织AMPK信号通路的作用机制
- Effect and Mechanism of Apigenin on Fat Metabolism Disorder AMPK Signaling Way in Obese Mice
- 中国实验方剂学杂志 2018年24卷第10期页码：107-111
- 作者机构：
- 作者简介：
- 基金信息：
  
  广东省自然科学基金项目（2015A030310222）
- DOI：10.13422/j.cnki.syfjx.20180816
  中图分类号： R285.5
- 纸质出版日期：2018
- 稿件说明：
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黄链莎, 刘铜华, 孙文, 等. 芹菜素对肥胖型小鼠脂肪组织AMPK信号通路的作用机制[J]. 中国实验方剂学杂志, 2018,24(10):107-111.

HUANG Lian-sha, LIU Tong-hua, SUN Wen, et al. Effect and Mechanism of Apigenin on Fat Metabolism Disorder AMPK Signaling Way in Obese Mice[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(10): 107-111.
黄链莎, 刘铜华, 孙文, 等. 芹菜素对肥胖型小鼠脂肪组织AMPK信号通路的作用机制[J]. 中国实验方剂学杂志, 2018,24(10):107-111. DOI： 10.13422/j.cnki.syfjx.20180816.

HUANG Lian-sha, LIU Tong-hua, SUN Wen, et al. Effect and Mechanism of Apigenin on Fat Metabolism Disorder AMPK Signaling Way in Obese Mice[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(10): 107-111. DOI： 10.13422/j.cnki.syfjx.20180816.

摘要

目的：研究芹菜素对肥胖型db/db小鼠脂肪紊乱的作用及机制。方法：8周龄雄性db/db小鼠随机分为模型组、芹菜素组（50 mg·kg-1·d-1），雄性C57BL/6J小鼠为正常组，药物干预4周后，检测小鼠体质量、空腹血糖（fasting blood glucose，FBG），总胆固醇（total cholesterol，CHO），甘油三酯（total triglyceride，TG），游离脂肪酸（free fatty acids，FFA），天冬氨酸氨基转移酶（aspartate aminotransferase，AST），血肌酐（serum creatinine，SCr），血尿素氮（blood urea nitrogen，BUN）；脂肪组织苏木素-伊红染色（hematoxylin-eosin staining，HE）观察脂肪细胞病理变化；实时荧光定量PCR（Real-time PCR）检测胆固醇应答元件结合蛋白1c（sterol regulatory element-binding protein 1c，SREBP1c），脂肪酸合成酶（fatty acid synthetase，FAS），过氧化物增殖物激活受体α（peroxisome proliferator activated receptor α，PPARα）基因表达；蛋白免疫印迹法（Western blot）检测腺苷酸活化蛋白激酶（phosphorylated adenosine monophosphate activated protein kinase，AMPK）和乙酰CoA羧化酶（acetyl-CoA carboxylase，ACC）磷酸化水平。结果：与模型组比较，芹菜素组小鼠体质量，FBG，CHO，TG，FFA明显降低（P<0.05，P<0.01）；HE染色脂肪细胞变小，脂质沉积减低；脂肪组织SREBP1c，FAS mRNA表达降低（P<0.01），p-AMPKα，p-ACC蛋白表达升高（P<0.05，P<0.01）。结论：芹菜素可以改善db/db小鼠脂肪代谢紊乱，可能是通过上调脂肪组织AMPK，ACC磷酸化水平，下调SREBP1c，FAS mRNA表达实现。

Abstract

Objective: To investigate the effect and mechanism of apigenin on fat metabolism disorder in Obese mice. Method: Eight-week-old male db/db mice were randomly divided into two groups

namely control group and apigenin group (50 mg·kg-1·d-1)

and 8 mice were used in each group. Another 8 male C57BL/6J mice were used as normal group. Body weight

serum glucose

lipid

histopathology and mRNA and protein expressions after a 4-week treatment were measured. Result: Compared with control group

apigenin group show significant decreases in body weight

fasting blood glucose (FBG)

total cholesterol (CHO)

total triglyceride (TG)

free fatty acids (FFA)

liver weight of mice (P<0.05

P<0.01)

and increases in fat deposition of adipose tissue according to the histological examination. The expressions of peroxisome proliferator activated receptor α (PPARα)

fatty acid synthetase (FAS) mRNA in adipose tissue of apigenin group decreased (P<0.01)

and the protein expressions of p-phosphorylated adenosine monophosphate activated protein kinaseα (AMPKα) and p-acetyl-CoA carboxylase (ACC) were significantly increased (P<0.01). Conclusion: The effect of apigenin in improving fatty metabolism of db/db mice may be realized by up-regulating the phosphorylation of AMPK and ACC and down-regulating the expressions of SREBP1c

FAS mRNA in adipose tissue.

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