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环氧化朴酚II通过丝裂原活化蛋白激酶介导的人骨髓间充质基质细胞中过氧化物酶体增殖物激活受体表达的抑制发挥抗脂肪生成特性。

Hyunganol II Exerts Antiadipogenic Properties via MAPK-Mediated Suppression of PPAR Expression in Human Bone Marrow-Derived Mesenchymal Stromal Cells.

作者信息

Oh Jung Hwan, Karadeniz Fatih, Seo Youngwan, Kong Chang-Suk

机构信息

Marine Biotechnology Center for Pharmaceuticals and Foods, College of Medical and Life Sciences, Silla University, Busan 46958, Republic of Korea.

Nutritional Education, Graduate School of Education, Silla University, Busan 46958, Republic of Korea.

出版信息

Evid Based Complement Alternat Med. 2022 Oct 17;2022:4252917. doi: 10.1155/2022/4252917. eCollection 2022.

DOI:10.1155/2022/4252917
PMID:36299776
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9592193/
Abstract

Bone marrow adiposity has been associated with several metabolic syndromes such as diabetes and osteoporosis. Imbalance in adipogenic and osteoblastogenic differentiation of human bone marrow mesenchymal stromal cells (hBM-MSCs) was suggested to be the cause of elevated bone marrow adiposity. There are several drugs, of both natural and synthetic origin, to treat bone loss. In this study, as a part of a recent trend to discover natural products with more biocompatibility and fewer side effects to treat bone loss, the effect of hyunganol II (HNG), a coumarin isolated from , on hBM-MSC adipogenesis was investigated. Cells treated with HNG showed decreased lipid accumulation indicating a diminished adipocyte phenotype. Treatment with HNG also suppressed the mRNA and protein expressions of PPAR, C/EBP, and SREBP1c, and three adipogenic marker genes. Further analysis of MAPK signaling pathway exhibited that HNG treatment elevated ERK activation and suppressed the JNK-mediated cFos and cJun phosphorylation, which inhibits PPAR transcriptional activity. Taken together, HNG treatment was shown to inhibit adipogenesis via suppressed PPAR expression as a result of altered MAPK signaling. Therefore, it was suggested that HNG might prevent bone marrow adiposity by inhibiting hBM-MSC adipogenesis and can be utilized as a drug or nutraceutical with beneficial effects on bone. Thus, further studies should be conducted to analyze its effect in vivo.

摘要

骨髓脂肪过多与多种代谢综合征有关,如糖尿病和骨质疏松症。人类骨髓间充质基质细胞(hBM-MSCs)的脂肪生成和成骨细胞分化失衡被认为是骨髓脂肪过多增加的原因。有几种天然和合成来源的药物可用于治疗骨质流失。在本研究中,作为发现具有更高生物相容性和更少副作用的天然产物来治疗骨质流失这一最新趋势的一部分,研究了从 中分离出的香豆素二氢山奈酚(HNG)对hBM-MSC脂肪生成的影响。用HNG处理的细胞显示脂质积累减少,表明脂肪细胞表型减弱。用HNG处理还抑制了PPAR、C/EBP和SREBP1c以及三个脂肪生成标记基因的mRNA和蛋白质表达。对MAPK信号通路的进一步分析表明,HNG处理提高了ERK激活,并抑制了JNK介导的cFos和cJun磷酸化,从而抑制了PPAR转录活性。综上所述,HNG处理通过改变MAPK信号导致PPAR表达受抑制,从而抑制脂肪生成。因此,有人提出HNG可能通过抑制hBM-MSC脂肪生成来预防骨髓脂肪过多,并可作为对骨骼有有益作用的药物或营养保健品。因此,应进一步开展研究以分析其体内作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c48/9592193/0e1f6c79f858/ECAM2022-4252917.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c48/9592193/a2518040cf57/ECAM2022-4252917.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c48/9592193/55ae8c7505d6/ECAM2022-4252917.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c48/9592193/4c10c72c7a15/ECAM2022-4252917.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c48/9592193/0e1f6c79f858/ECAM2022-4252917.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c48/9592193/a2518040cf57/ECAM2022-4252917.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c48/9592193/55ae8c7505d6/ECAM2022-4252917.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c48/9592193/4c10c72c7a15/ECAM2022-4252917.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c48/9592193/0e1f6c79f858/ECAM2022-4252917.004.jpg

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