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从 3T3-L1 脂肪细胞中分离得到的 α-古巴醇的抗肥胖作用。

Anti-Obesity Effect of α-Cubebenol Isolated from in 3T3-L1 Adipocytes.

机构信息

Department of Biomaterials Science (BK21 FOUR Program), Life and Industry Convergence Research Institute, College of Natural Resources and Life Science, Pusan National University, Miryang 50463, Korea.

Department of Horticultural Bioscience, Life and Industry Convergence Research Institute, College of Natural Resources & Life Science, Pusan National University, Miryang 50463, Korea.

出版信息

Biomolecules. 2021 Nov 8;11(11):1650. doi: 10.3390/biom11111650.

Abstract

The efficacy of α-cubebenol isolated from has been studied in several diseases, including cecal ligation, puncture challenge-induced sepsis, and degranulation of neutrophils. To identify the novel functions of α-cubebenol on lipid metabolism, alterations on the regulation of lipogenesis, lipolysis, and inflammatory response were observed in 3T3-L1 adipocytes treated with α-cubebenol. Most lipogenic targets, including lipid accumulation, level of lipogenic transcription factors, and expression of lipogenic regulators, were suppressed in MDI (3-isobutyl-1-methylxanthine, dexamethasone, and insulin)-stimulated 3T3-L1 adipocytes treated with α-cubebenol without significant cytotoxicity. In addition, similar inhibition effects were observed in the iNOS-induced COX-2 mediated pathway and NLRP3 inflammasome pathway of MDI-stimulated 3T3-L1 cells treated with α-cubebenol. Lipolytic targets, such as cAMP concentration, expression of adenylyl cyclase and PDE4, and their downstream signaling pathway, in MDI-stimulated 3T3-L1 cells were stimulated by the α-cubebenol treatment. The levels of transcription factors and related proteins for β-oxidation were significantly higher in the MDI + α-cubebenol treated group than in the MDI + Vehicle treated group. These results show that α-cubebenol has a novel role as a lipogenesis inhibitor, lipolysis and β-oxidation stimulator, and inflammasome suppressor in MDI-stimulated 3T3-L1 adipocytes.

摘要

从 中分离得到的 α-古巴醇在几种疾病中的疗效已经得到了研究,包括盲肠结扎和穿孔打击诱导的脓毒症,以及中性粒细胞脱颗粒。为了确定 α-古巴醇在脂质代谢方面的新功能,在 3T3-L1 脂肪细胞中观察到 α-古巴醇处理后脂生成的调节、脂肪分解和炎症反应的变化。在 MDI(3-异丁基-1-甲基黄嘌呤、地塞米松和胰岛素)刺激的 3T3-L1 脂肪细胞中,大多数脂生成靶标,包括脂质积累、脂生成转录因子水平和脂生成调节剂的表达,均被 α-古巴醇抑制,而没有明显的细胞毒性。此外,在 MDI 刺激的 3T3-L1 细胞中,iNOS 诱导的 COX-2 介导途径和 NLRP3 炎性体途径中也观察到类似的抑制作用。在 MDI 刺激的 3T3-L1 细胞中,α-古巴醇处理还刺激了脂解靶标,如 cAMP 浓度、腺苷酸环化酶和 PDE4 的表达及其下游信号通路。在 MDI+α-古巴醇处理组中,β-氧化的转录因子和相关蛋白水平明显高于 MDI+Vehicle 处理组。这些结果表明,α-古巴醇在 MDI 刺激的 3T3-L1 脂肪细胞中具有作为脂生成抑制剂、脂肪分解和β-氧化刺激剂以及炎性体抑制剂的新作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8728/8615670/d672c36b2343/biomolecules-11-01650-g001.jpg

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