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从何首乌中分离得到的 Polygalin C 通过抑制 3T3-L1 脂肪细胞中成脂和成脂因子发挥抗肥胖作用。

Anti-Obesity Effect of Polygalin C Isolated from Houtt. via Suppression of the Adipogenic and Lipogenic Factors in 3T3-L1 Adipocytes.

机构信息

College of Korean Medicine, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea.

Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Seoul 02447, Korea.

出版信息

Int J Mol Sci. 2021 Sep 27;22(19):10405. doi: 10.3390/ijms221910405.

Abstract

Obesity is a risk factor for metabolic diseases including type 2 diabetes, nonalcoholic steatohepatitis (NASH), heart diseases, and cancer. This study aimed to investigate the anti-obesity effect of Polygalin C (PC) isolated from Houtt. in 3T3-L1 adipocytes. Based on Oil Red O assay results, PC significantly decreased lipid accumulation compared to the control. We found that PC suppressed adipogenesis transcription factors including peroxisome proliferator-activated receptor γ (PPAR γ) and CCAAT/enhancer-binding protein (C/EBP) α, and lipogenic factors such as sterol regulatory element-binding protein 1c (SREBP 1c) and fatty acid synthase (FAS), in 3T3-L1 adipocytes using Western blotting and real-time polymerase chain reaction (PCR). Moreover, PC inhibited the differentiation of 3T3-L1 cells by regulating the AMP-activated protein kinase (AMPK)/acetyl-CoA carboxylase (ACC) and mitogen-activated protein kinase/protein kinase B (MAPK/Akt) signaling pathways. Additionally, we confirmed that PC inhibited early adipogenesis factors C/EBP β and C/EBP δ. Therefore, PC inhibited adipogenesis and lipogenesis in vitro. Thus, PC appears to exert potential therapeutic effects on obesity by suppressing lipid metabolism.

摘要

肥胖是包括 2 型糖尿病、非酒精性脂肪性肝炎(NASH)、心脏病和癌症在内的代谢性疾病的一个风险因素。本研究旨在探究从 Houtt. 中分离得到的 Polygalin C(PC)在 3T3-L1 脂肪细胞中抗肥胖的作用。根据油红 O 染色试验的结果,PC 与对照组相比显著减少了脂肪堆积。我们发现,PC 通过 Western blot 和实时聚合酶链反应(PCR)抑制了脂肪生成转录因子,包括过氧化物酶体增殖物激活受体 γ(PPARγ)和 CCAAT/增强子结合蛋白(C/EBP)α,以及固醇调节元件结合蛋白 1c(SREBP 1c)和脂肪酸合酶(FAS)等脂肪生成因子,在 3T3-L1 脂肪细胞中。此外,PC 通过调节 AMP 激活的蛋白激酶(AMPK)/乙酰辅酶 A 羧化酶(ACC)和丝裂原激活的蛋白激酶/蛋白激酶 B(MAPK/Akt)信号通路抑制了 3T3-L1 细胞的分化。此外,我们还证实,PC 抑制了早期脂肪生成因子 C/EBPβ和 C/EBPδ。因此,PC 在体外抑制脂肪生成和脂肪生成。因此,PC 通过抑制脂质代谢,对肥胖症似乎具有潜在的治疗作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/716c/8508696/cdd28322b83e/ijms-22-10405-g001.jpg

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