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从藤五加(Acanthopanax henryi (Oliv.) Harms)叶中分离得到的糖苷St-E2和糖苷St-C1对3T3-L1细胞的抗脂肪生成作用

Anti-adipogenic effect of Glycoside St-E2 and Glycoside St-C1 isolated from the leaves of Acanthopanax henryi (Oliv.) Harms in 3T3-L1 cells.

作者信息

Han Yo-Han, Li Zhi, Um Jae-Young, Liu Xiang Qian, Hong Seung-Heon

机构信息

a Department of Oriental Pharmacy, College of Pharmacy, Wonkwang-Oriental Medicines Research Institute , Wonkwang University , Iksan , Republic of Korea.

b School of Pharmacy , Hunan University of Chinese Medicine , Changsha , China.

出版信息

Biosci Biotechnol Biochem. 2016 Dec;80(12):2391-2400. doi: 10.1080/09168451.2016.1217150. Epub 2016 Aug 5.

DOI:10.1080/09168451.2016.1217150
PMID:27494072
Abstract

Acanthopanax henryi (Oliv.) Harms has been used in the treatment of arthritis, rheumatism, and abdominal pain. This study evaluated whether natural compounds isolated from the leaves of A. henryi (Oliv.) Harms could inhibit adipocyte differentiation by regulating transcriptional factors such as peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα). AMP-activated protein kinase (AMPK) activity was also evaluated. Among the several compounds isolated from the leaves of A. henryi (Oliv.) Harms, Glycoside St-C1 and Glycoside St-E2 significantly decreased lipid accumulation and the expressions of PPARγ and C/EBPα. Glycoside St-C1 and Glycoside St-E2 were found to activate AMPK when they regulated PPARγ and C/EBPα. Results confirmed that Glycoside St-C1 and Glycoside St-E2 isolated from the leaves of A. henryi (Oliv.) Harms can inhibit adipogenesis through the AMPK-PPARγ-C/EBPα mechanism. Thus, this study suggests that Glycoside St-C1 and Glycoside St-E2 have a therapeutic effect due to activation of the AMPKα.

摘要

藤五加已被用于治疗关节炎、风湿病和腹痛。本研究评估了从藤五加叶中分离出的天然化合物是否能通过调节转录因子如过氧化物酶体增殖物激活受体γ(PPARγ)和CCAAT/增强子结合蛋白α(C/EBPα)来抑制脂肪细胞分化。同时也评估了AMP激活的蛋白激酶(AMPK)活性。从藤五加叶中分离出的几种化合物中,糖苷St-C1和糖苷St-E2显著降低了脂质积累以及PPARγ和C/EBPα的表达。发现糖苷St-C1和糖苷St-E2在调节PPARγ和C/EBPα时能激活AMPK。结果证实,从藤五加叶中分离出的糖苷St-C1和糖苷St-E2可通过AMPK-PPARγ-C/EBPα机制抑制脂肪生成。因此,本研究表明,糖苷St-C1和糖苷St-E2由于激活了AMPKα而具有治疗作用。

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