柏柏林通过调解PPARδ的转录功能来减少肥胖中的脂质积累
Jia-Wen Shou1,2, Pang-Chui Shaw1,2,3
1Li Dak Sum Yip Yio Chin R&D Centre for Chinese Medicine, The Chinese University of Hong Kong, Hong Kong, China.
International journal of molecular sciences
|July 29, 2023
概括
来自Coptidis Rhizoma的柏柏林 (BBR) 通过激活Peroxisome增殖器激活受体三角 (PPARδ) 来减少肥胖. 这种机制降低了脂质积累,并改善了肥胖模型中的代谢标志物.
科学领域:
- 药理学 药理学是指药理学的学科.
- 代谢疾病 代谢疾病
- 传统中国医药 传统中国医药
背景情况:
- 肥胖症在中国传统医学中被描述为湿热综合征.
- 科普蒂迪斯树根及其活性化合物柏柏林 (BBR) 用于治疗肥胖症.
- 过氧体增殖器激活受体 (PPAR) 调节新陈代谢,但它们在BBR抗肥胖作用中的作用尚不清楚.
研究的目的:
- 调查PPARs在BBR的抗肥胖作用中的作用.
- 阐明BBR对肥胖的作用背后的分子机制.
主要方法:
- 在BBR治疗后,对PPAR亚型 (PPARα,PPARγ,PPARδ) 水平的剂量依赖性分析.
- 基因沉默和对抗剂研究以确定关键的PPAR亚型.
- 在体外研究使用3T3L1前脂质细胞来评估脂质积累.
- 使用高脂肪饮食 (HFD) 诱导的肥胖小鼠进行体内研究,以评估体重增加,脂肪组织质量和生物化学参数.
- 检查PPARδ激活和下游基因调节的机制研究.
主要成果:
- BBR剂量依赖调节PPARγ和PPARδ,但不是PPARα.
- 确定PPARδ对于BBR的抗肥胖作用至关重要.
- 在HFD小鼠中,BBR减少了3T3L1细胞中的脂质积累,减轻了体重增加,白色脂肪组织质量,改善了脂质,炎症和氧化标志物.
- BBR的影响被PPARδ抗剂逆转.
- BBR激活了PPARδ,对其下游基因进行了上调,并调节了Cebpα,Pparγ和Ho-1的促进剂.
结论:
- 这项研究揭示了PPARδ介导的BBR的新型抗肥胖机制.
- BBR激活PPARδ,导致脂质积累减少和改善代谢健康.
- 这些发现支持BBR作为通过PPARδ激活来治疗肥胖的潜在治疗剂.
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