金松酸对高脂饮食诱导的肥胖小鼠肝脏脂质代谢的影响

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

目的:本研究旨在探究金松酸(sciadonic acid,SA)对高脂饮食诱导小鼠肥胖的改善作用。方法:将48只C57BL/6雄鼠适应性喂养一周后随机分为正常组(C)、阳性对照组(S)、模型组(M)、金松酸低剂量组(LSA)、金松酸中剂量组(MSA)和金松酸高剂量组(HSA)。造模和给药同时进行,持续16周,低、高剂量组每日固定时间灌胃不同剂量的金松酸溶液。实验结束后从血脂代谢、肝脏脂肪代谢、肝脏氧化应激、肝脏脂质合成和代谢相关基因的表达等几个方面探讨金松酸调节肥胖小鼠脂质代谢的潜在机制。结果表明,高剂量金松酸干预肥胖小鼠能显著降低血清中总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)含量,增加高密度脂蛋白胆固醇(HDL-C)(P<0.05),抑制体重增长,减少附睾脂肪积累,对肝组织损伤具有改善作用。此外,金松酸能明显提高小鼠体内超氧化物歧化酶(SOD)、谷胱甘肽过氧化酶(GSH-Px)等抗氧化酶的活性(P<0.05),并显著降低氧化终产物MDA的生成(P<0.05),缓解体内氧化应激反应,并通过调节脂质代谢相关基因的表达,抑制脂质合成,改善脂质代谢。综上,金松酸可通过抑制脂肪积累,缓解氧化应激,调控脂质合成和代谢改善肥胖小鼠脂质代谢紊乱。

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.