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扁柏酚介导的AMPK激活通过自噬通量抑制间充质干细胞的成脂分化。

AMPK Activation Mediated by Hinokitiol Inhibits Adipogenic Differentiation of Mesenchymal Stem Cells through Autophagy Flux.

作者信息

Lee Ju-Hee, Jeong Jae-Kyo, Park Sang-Youel

机构信息

Biosafety Research Institute, College of Veterinary Medicine, Chonbuk National University, Iksan, Jeonbuk 54596, Republic of Korea.

New Drug Development Center, Daegu-Gyeongbuk Medical Innovation Foundation, 88 Dongnae-ro, Dong-gu, Daegu City 41061, Republic of Korea.

出版信息

Int J Endocrinol. 2018 Jul 10;2018:2014192. doi: 10.1155/2018/2014192. eCollection 2018.

DOI:10.1155/2018/2014192
PMID:30123258
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6079415/
Abstract

BACKGROUND AND PURPOSE

Hinokitiol, a natural monopenoid present in the essential oil of heartwood, exerts potent anticancer, anti-inflammatory, antibacterial, and neuroprotective effects on various cells. However, the antiobesity effect of hinokitiol on adipocytes is unclear.

EXPERIMENTAL APPROACH

In this study, we observed that hinokitiol affected the differentiation to adipocytes in mesenchymal stem cells (MSCs). Hinokitiol was treated with 3-isobutyl-1-methylxanthine, insulin, and dexamethasone to induce differentiation and maturing adipocytes in cultured MSCs.

KEY RESULTS

Hinokitiol treatment of MSCs decreased their differentiation to mature adipocytes and increased AMPK phosphorylation in a concentration-dependent manner. Moreover, we confirmed that the antiadipogenic effect of hinokitiol was associated with autophagy. The levels of LC3-II decreased and those of p62 increased in hinokitiol-treated MSCs. The treatment of hinokitiol-treated MSCs with the autophagy activator, rapamycin, restored the hinokitiol-induced decrease in the adipocyte differentiation of MSCs. The inhibition of AMPK phosphorylation also suppressed hinokitiol-mediated inhibition of autophagy and antiadipogenic effects.

CONCLUSIONS AND IMPLICATIONS

Taken together, these results indicated that AMPK activation and autophagy flux inhibition mediated by hinokitiol inhibited lipid accumulation and differentiation of MSCs to adipocytes and also suggest that differentiation of mesenchymal stem cells may be regulated by using the modulator of autophagy flux and AMPK signals including hinokitiol.

摘要

背景与目的

扁柏酚是一种存在于心材精油中的天然单萜类化合物，对多种细胞具有强大的抗癌、抗炎、抗菌和神经保护作用。然而，扁柏酚对脂肪细胞的抗肥胖作用尚不清楚。

实验方法

在本研究中，我们观察到扁柏酚影响间充质干细胞（MSC）向脂肪细胞的分化。用3-异丁基-1-甲基黄嘌呤、胰岛素和地塞米松处理扁柏酚，以诱导培养的MSC中脂肪细胞的分化和成熟。

关键结果

用扁柏酚处理MSC可降低其向成熟脂肪细胞的分化，并以浓度依赖的方式增加AMPK磷酸化。此外，我们证实扁柏酚的抗脂肪生成作用与自噬有关。在经扁柏酚处理的MSC中，LC3-II水平降低，p62水平升高。用自噬激活剂雷帕霉素处理经扁柏酚处理的MSC，可恢复扁柏酚诱导的MSC脂肪细胞分化减少。抑制AMPK磷酸化也抑制了扁柏酚介导的自噬抑制和抗脂肪生成作用。

结论与启示

综上所述，这些结果表明，扁柏酚介导的AMPK激活和自噬通量抑制可抑制MSC脂质积累和向脂肪细胞的分化，也提示间充质干细胞的分化可能通过使用包括扁柏酚在内的自噬通量和AMPK信号调节剂来调节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b13/6079415/02d0f2a8d7c3/IJE2018-2014192.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b13/6079415/9805be1e6707/IJE2018-2014192.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b13/6079415/6356cbb91ac8/IJE2018-2014192.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b13/6079415/0691267837a5/IJE2018-2014192.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b13/6079415/1d4ae361d431/IJE2018-2014192.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b13/6079415/938bea0f179a/IJE2018-2014192.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b13/6079415/02d0f2a8d7c3/IJE2018-2014192.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b13/6079415/9805be1e6707/IJE2018-2014192.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b13/6079415/6356cbb91ac8/IJE2018-2014192.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b13/6079415/0691267837a5/IJE2018-2014192.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b13/6079415/1d4ae361d431/IJE2018-2014192.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b13/6079415/938bea0f179a/IJE2018-2014192.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b13/6079415/02d0f2a8d7c3/IJE2018-2014192.006.jpg

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