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中國精品科技期刊2020
楊興文,姚詩煒,盧紅伶,等. 金松酸對高脂飲食誘導的肥胖小鼠肝臟脂質代謝的影響[J]. 食品工業科技,2024,45(6):304?312. doi: 10.13386/j.issn1002-0306.2023040023.
引用本文: 楊興文,姚詩煒,盧紅伶,等. 金松酸對高脂飲食誘導的肥胖小鼠肝臟脂質代謝的影響[J]. 食品工業科技,2024,45(6):304?312. doi: 10.13386/j.issn1002-0306.2023040023.
YANG Xingwen, YAO Shiwei, LU Hongling, et al. Effect of Sciadonic Acid on Hepatic Lipid Metabolism in Obese Mice Induced by A High-fat Diet[J]. Science and Technology of Food Industry, 2024, 45(6): 304?312. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2023040023.
Citation: YANG Xingwen, YAO Shiwei, LU Hongling, et al. Effect of Sciadonic Acid on Hepatic Lipid Metabolism in Obese Mice Induced by A High-fat Diet[J]. Science and Technology of Food Industry, 2024, 45(6): 304?312. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2023040023.

金松酸對高脂飲食誘導的肥胖小鼠肝臟脂質代謝的影響

Effect of Sciadonic Acid on Hepatic Lipid Metabolism in Obese Mice Induced by A High-fat Diet

  • 摘要: 目的:本研究旨在探究金松酸(sciadonic acid,SA)對高脂飲食誘導小鼠肥胖的改善作用。方法:將48只C57BL/6雄鼠適應性喂養一周后隨機分為正常組(C)、陽性對照組(S)、模型組(M)、金松酸低劑量組(LSA)、金松酸中劑量組(MSA)和金松酸高劑量組(HSA)。造模和給藥同時進行,持續16周,低、高劑量組每日固定時間灌胃不同劑量的金松酸溶液。實驗結束后從血脂代謝、肝臟脂肪代謝、肝臟氧化應激、肝臟脂質合成和代謝相關基因的表達等幾個方面探討金松酸調節肥胖小鼠脂質代謝的潛在機制。結果表明,高劑量金松酸干預肥胖小鼠能顯著降低血清中總膽固醇(TC)、甘油三酯(TG)、低密度脂蛋白膽固醇(LDL-C)含量,增加高密度脂蛋白膽固醇(HDL-C)(P<0.05),抑制體重增長,減少附睪脂肪積累,對肝組織損傷具有改善作用。此外,金松酸能明顯提高小鼠體內超氧化物歧化酶(SOD)、谷胱甘肽過氧化酶(GSH-Px)等抗氧化酶的活性(P<0.05),并顯著降低氧化終產物MDA的生成(P<0.05),緩解體內氧化應激反應,并通過調節脂質代謝相關基因的表達,抑制脂質合成,改善脂質代謝。綜上,金松酸可通過抑制脂肪積累,緩解氧化應激,調控脂質合成和代謝改善肥胖小鼠脂質代謝紊亂。

     

    Abstract: Objective: To investigate the potential beneficial effects of sciadonic acid (SA) on improving obesity induced by a high-fat diet in mice. Methods: Forty-eight male C57BL/6 mice were adaptively fed for one week and then randomly divided into the following groups: Control group (C), positive control group (S), model group (M), low-dose sciadonic acid group (LSA), medium-dose sciadonic acid group (MSA), and high-dose sciadonic acid group (HSA). The modeling process lasted for 16 weeks, and the low and high-dose groups were orally administered different doses of SA solution at a fixed time each day. After the modeling period, potential mechanisms of SA in regulating lipid metabolism in obese mice were explored, including aspects such as blood lipid metabolism, hepatic fat metabolism, hepatic oxidative stress, hepatic lipid synthesis, and expression of metabolism-related genes. Results: The high-dose SA intervention in obese mice significantly decreased the levels of total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C) in serum, while increasing high-density lipoprotein cholesterol (HDL-C) (P<0.05). It inhibited weight gain, reduced epididymal fat accumulation, and improved liver tissue damage. Additionally, SA significantly increased the activities of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in mice (P<0.05), and significantly reduced the production of oxidative end products MDA (P<0.05), alleviated oxidative stress in vivo, and inhibited lipid synthesis by regulating the expression of genes related to lipid metabolism to improve lipid metabolism. Conclusion: SA could improve lipid metabolism disorders in obese mice by suppressing fat accumulation, alleviate oxidative stress, regulate lipid synthesis and metabolism.

     

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