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中长链甘油三酯丙泊酚降低HepG2和Huh7细胞肝脂质代谢中乙酰辅酶A羧化酶的活性。

Medium- and long-chain triglyceride propofol reduces the activity of acetyl-coenzyme A carboxylase in hepatic lipid metabolism in HepG2 and Huh7 cells.

作者信息

Wang Li-Yuan, Wu Jing, Gao Ya-Fen, Lin Duo-Mao, Ma Jun

机构信息

Center for Anesthesiology, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, P.R China.

North China University of Science and Technology, Tangshan, Hebei 063300, P.R China.

出版信息

Korean J Physiol Pharmacol. 2020 Jan;24(1):19-26. doi: 10.4196/kjpp.2020.24.1.19. Epub 2020 Dec 20.

Abstract

Medium- and long-chain triglyceride (MCT/LCT) propofol is widely used as an intravenous anesthetic, especially in the intensive care unit. The present study aimed to assess whether MCT/LCT propofol is safe in the hyperlipidemic population for long-term use. Free fatty acids (FFAs) were used to establish high-fat stimulation of HepG2 and Huh7 cells. Subsequently, these cells were treated with propofol at the concentration of 0, 4, or 8 µg/ml for 24 and 48 h. The results indicated that the cell viability was notably decreased when the cells were stimulated with 2 mmol/L FFAs and treated with 12 µg/ml MCT/LCT propofol. Accordingly, we chose 2 mmol/L FFAs along with 4 and 8 µg/ml MCT/LCT propofol for the subsequent experiments. Four and 8 µg/ml MCT/LCT propofol inhibited FFA-induced lipid accumulation in the cells and significantly reversed acetyl coenzyme A carboxylase (ACC) activity. In addition, MCT/LCT propofol not only significantly promoted the phosphorylation of AMPK and ACC, but also reversed the FFA-induced decreased phosphorylation of AMPK and ACC. In conclusion, MCT/LCT propofol reverses the negative effects caused by FFAs in HepG2 and Huh7 cells, indicating that MCT/LCT propofol might positively regulate lipid metabolism.

摘要

中长链甘油三酯(MCT/LCT)丙泊酚作为一种静脉麻醉剂被广泛应用,尤其是在重症监护病房。本研究旨在评估MCT/LCT丙泊酚在高脂血症人群中长期使用是否安全。使用游离脂肪酸(FFA)对HepG2和Huh7细胞建立高脂刺激。随后,将这些细胞分别用浓度为0、4或8μg/ml的丙泊酚处理24小时和48小时。结果表明,当细胞用2mmol/L FFA刺激并同时用12μg/ml MCT/LCT丙泊酚处理时,细胞活力显著降低。因此,我们选择2mmol/L FFA以及4和8μg/ml MCT/LCT丙泊酚用于后续实验。4和8μg/ml MCT/LCT丙泊酚抑制了FFA诱导的细胞内脂质积累,并显著逆转了乙酰辅酶A羧化酶(ACC)的活性。此外,MCT/LCT丙泊酚不仅显著促进了AMPK和ACC的磷酸化,还逆转了FFA诱导的AMPK和ACC磷酸化降低。总之,MCT/LCT丙泊酚逆转了FFA对HepG2和Huh7细胞造成的负面影响,表明MCT/LCT丙泊酚可能对脂质代谢具有正向调节作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d59/6940496/2aaf7d42470c/kjpp-24-19-g001.jpg

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