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蜂毒通过抑制脂肪生成抑制前脂肪细胞的分化和高脂饮食诱导的肥胖。

Bee Venom Suppresses the Differentiation of Preadipocytes and High Fat Diet-Induced Obesity by Inhibiting Adipogenesis.

机构信息

Department of Pharmacology, College of Korean Medicine, Sang-ji University, Wonju-si, Gangwon-do 26339, Korea.

Catholic Precision Medicine Research Center, College of Medicine, The Catholic University of Korea, 222, Banpo-daero, Seocho-gu, Seoul 06591, Korea.

出版信息

Toxins (Basel). 2017 Dec 24;10(1):9. doi: 10.3390/toxins10010009.

DOI:10.3390/toxins10010009
PMID:29295544
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5793096/
Abstract

Bee venom (BV) has been widely used in the treatment of certain immune-related diseases. It has been used for pain relief and in the treatment of chronic inflammatory diseases. Despite its extensive use, there is little documented evidence to demonstrate its medicinal utility against obesity. In this study, we demonstrated the inhibitory effects of BV on adipocyte differentiation in 3T3-L1 cells and on a high fat diet (HFD)-induced obesity mouse model through the inhibition of adipogenesis. BV inhibited lipid accumulation, visualized by Oil Red O staining, without cytotoxicity in the 3T3-L1 cells. Male C57BL/6 mice were fed either a HFD or a control diet for 8 weeks, and BV (0.1 mg/kg or 1 mg/kg) or saline was injected during the last 4 weeks. BV-treated mice showed a reduced body weight gain. BV was shown to inhibit adipogenesis by downregulating the expression of the transcription factors CCAAT/enhancer-binding proteins (C/EBPs) and the peroxisome proliferator-activated receptor gamma (PPARγ), using RT-qPCR and Western blotting. BV induced the phosphorylation of AMP-activated kinase (AMPK) and acetyl-CoA carboxylase (ACC) in the cell line and in obese mice. These findings demonstrate that BV mediates anti-obesity/differentiation effects by suppressing obesity-related transcription factors.

摘要

蜂毒 (BV) 已广泛用于治疗某些与免疫相关的疾病。它已被用于缓解疼痛和治疗慢性炎症性疾病。尽管它被广泛使用,但几乎没有文献证据证明它对肥胖症具有药用价值。在这项研究中,我们通过抑制脂肪生成,证明了 BV 对 3T3-L1 细胞中脂肪细胞分化和高脂肪饮食 (HFD) 诱导肥胖小鼠模型的抑制作用。BV 在不具有细胞毒性的情况下抑制了 3T3-L1 细胞中的脂质积累,通过油红 O 染色可见。雄性 C57BL/6 小鼠连续 8 周喂食 HFD 或对照饮食,在最后 4 周注射 BV(0.1mg/kg 或 1mg/kg)或生理盐水。BV 处理的小鼠体重增加减少。通过 RT-qPCR 和 Western blot 分析,BV 被证明通过下调转录因子 CCAAT/增强子结合蛋白 (C/EBP) 和过氧化物酶体增殖物激活受体 γ (PPARγ) 的表达来抑制脂肪生成。BV 在细胞系和肥胖小鼠中诱导 AMP 激活的蛋白激酶 (AMPK) 和乙酰辅酶 A 羧化酶 (ACC) 的磷酸化。这些发现表明,BV 通过抑制肥胖相关的转录因子来介导抗肥胖/分化作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd03/5793096/9f40ed34ce9b/toxins-10-00009-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd03/5793096/7c46895f42a2/toxins-10-00009-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd03/5793096/fd07de515b75/toxins-10-00009-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd03/5793096/dc82a4945a42/toxins-10-00009-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd03/5793096/ce3510723429/toxins-10-00009-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd03/5793096/9f40ed34ce9b/toxins-10-00009-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd03/5793096/7c46895f42a2/toxins-10-00009-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd03/5793096/fd07de515b75/toxins-10-00009-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd03/5793096/dc82a4945a42/toxins-10-00009-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd03/5793096/ce3510723429/toxins-10-00009-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd03/5793096/9f40ed34ce9b/toxins-10-00009-g005.jpg

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