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葎草能促进脂肪细胞产热并改善氧化应激。

Humulus japonicus stimulates thermogenesis and ameliorates oxidative stress in mouse adipocytes.

机构信息

Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea.

Neuropsychopharmacology and Toxicology Program, College of Pharmacy, Kangwon National University, Chunchon, Republic of Korea.

出版信息

J Mol Endocrinol. 2019 Jul 1;63(1):1-9. doi: 10.1530/JME-19-0010.

Abstract

An aqueous extract of Humulus japonicus (AH) has been documented to ameliorate hypertension and non-alcoholic fatty liver disease (NAFLD). Here, we investigated the effects of an aqueous extract of AH on thermogenesis and palmitate-induced oxidative stress in adipocytes. To verify the effect of AH on browning, we measured the expression levels of specific markers in 3T3-L1 adipocytes using qPCR and Western blotting, respectively. To assess the role of oxidative stress, cells were stained with DCFDA and observed by fluorescence microscopy. AH increased the expression of brown adipose tissue-specific markers. Additionally, it induced fatty acid oxidation and lipolysis and suppressed both lipogenic markers and lipid accumulation. Furthermore, AH ameliorated hydrogen peroxide-induced oxidative stress. Enhanced expression of these markers contributed to fat browning, fatty acid oxidation and lipolysis of 3T3-L1 adipocytes via the AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor delta (PPARδ) signaling pathways. Moreover, AMPK and PPARδ resulting in protective effects of AH against oxidative stress. In sum, AH could promote the browning, lipolysis and thermogenesis in 3T3-L1 adipocytes and would suppress the hydrogen peroxide-induced oxidative stress and lipogenesis during differentiation. We therefore suggest that AH could be used as a potential candidate for treating obesity and related metabolic disorders.

摘要

已发现葎草的水提物可改善高血压和非酒精性脂肪肝(NAFLD)。在这里,我们研究了葎草水提物对脂肪细胞产热和棕榈酸诱导的氧化应激的影响。为了验证 AH 对褐色变的影响,我们分别使用 qPCR 和 Western blot 测定了 3T3-L1 脂肪细胞中特定标志物的表达水平。为了评估氧化应激的作用,我们用 DCFDA 染色并用荧光显微镜观察细胞。AH 增加了褐色脂肪组织特异性标志物的表达。此外,它还诱导脂肪酸氧化和脂肪分解,并抑制脂肪生成标志物和脂质积累。此外,AH 改善了过氧化氢诱导的氧化应激。这些标志物的表达增强有助于 3T3-L1 脂肪细胞的脂肪褐色变、脂肪酸氧化和脂肪分解,这是通过 AMP 激活的蛋白激酶(AMPK)和过氧化物酶体增殖物激活受体δ(PPARδ)信号通路实现的。此外,AMPK 和 PPARδ 导致 AH 对氧化应激的保护作用。总之,AH 可促进 3T3-L1 脂肪细胞的褐色变、脂肪分解和产热,并抑制分化过程中过氧化氢诱导的氧化应激和脂肪生成。因此,我们认为 AH 可作为治疗肥胖症和相关代谢紊乱的潜在候选药物。

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