| 引用本文:高晶，魏益谦，孟智睿，邵紫萱，李丽，张建军，王景霞.沙苑子苷A对脂肪变L02细胞中三酰甘油水解及炎症介质的影响[J].世界中医药,2022,(17):. |
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| 沙苑子苷A对脂肪变L02细胞中三酰甘油水解及炎症介质的影响 |
| Effect of Complanatoside A on ATGL，PPARs，and Inflammatory Factors of Steatosis L02 Cells |
| 投稿时间：2021-02-11 |
| DOI：10.3969/j.issn.1673-7202.2022.17.011 |
| 中文关键词: 沙苑子 沙苑子苷A 高脂血症 L02细胞 细胞凋亡 三酰甘油 三酰甘油水解酶 过氧化物酶体增殖物激活受体 |
| English Keywords:Semen Astragali Complanati Complanatoside A Hyperlipidemia L02 cells Apoptosis TG ATGL PPAR |
| 基金项目:国家自然科学基金项目（81673617）——雌激素受体介导的沙苑子温阳化浊调节肝脏TG代谢的机制研究 |
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| 中文摘要: |
| 目的：研究沙苑子苷A对脂肪变L02细胞的降脂效果和作用机制。方法：采用游离脂肪酸（FFA）诱导肝L02细胞脂肪变性，分为对照组、模型组、沙苑子苷A低剂量、中剂量、高剂量组（1 μmol/L、10 μmol/L、50 μmol/L），流式细胞仪检测细胞凋亡和脂肪堆积，按照试剂盒检测三酰甘油（TG）、胆固醇（TC）、丙二醛（MDA）、超氧化物歧化酶（SOD）的水平，实时荧光定量PCR（qPCR）检测三酰甘油水解酶（ATGL）、过氧化物酶体增殖物激活受体α（PPAR-α）、过氧化物酶体增殖物激活受体γ（PPARγ）、肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）mRNA的表达，蛋白质印迹法（Western Blotting）检测ATGL、PPAR-α、PPARγ、TNF-α、IL-6蛋白的表达。结果：沙苑子苷A能显著减少脂肪堆积，降低TG、TC、MDA含量，增加SOD活性，降低细胞凋亡率，减轻脂毒性造成的肝细胞损伤，与模型组比较差异有统计学意义(P<0.05，P<0.01)；沙苑子苷A能升高ATGL、PPAR-α、PPARγmRNA和蛋白的表达，同时降低TNF-α、IL-6 mRNA和蛋白的表达，与模型组比较差异有统计学意义(P<0.01)。结论：沙苑子苷A可能通过上调PPARα、PPARγ的表达，使ATGL表达增加，促进肝脏TG的水解，减少肝脏脂肪的沉积，缓解氧化应激，抑制TNF-α和IL-６的分泌，减轻炎症反应，从而恢复肝细胞的正常功能。 |
| English Summary: |
| To study the hypolipidemic effect of complanatoside A on steatosis L02 cells and the mechanism.Methods:Free fatty acid(FFA) was used to induce steatosis in human liver L02 cells.The cells were classified into the blank group，model group，and low-dose，medium-dose，and high-dose complanatoside A groups(1 μmol/L，10 μmol/L，and 50 μmol/L，respectively).Apoptosis and fat accumulation were detected by flow cytometry.The levels of triglyceride(TG)，total cholesterol(TC)，malondialdehyde(MDA)，and superoxide dismutase(SOD) were determined with corresponding kits.The mRNA expression of adipose triglyceride lipase(ATGL)，peroxisome proliferator-activated receptor(PPAR)-α，PPAR-γ，tumor necrosis factor(TNF)-α，and interleukin-6(IL-6) was measured by qPCR，and the protein expression of ATGL，PPAR-α，PPARγ，TNF-α，and IL-6 by Western Blotting.Results:Complanatoside A reduced fat accumulation，content of TG，TC，and MDA，and apoptosis rate，enhanced SOD activity，and alleviated liver cell injury caused by lipotoxicity as compared with the model group(P<0.05，P<0.01).Complanatoside A raised the mRNA and protein expression of ATGL，PPAR-α，and PPARγ and lowered the mRNA and protein expression of TNF-α and IL-6 in comparison with the model group(P<0.01).Conclusion:Perhaps by up-regulating the expression of PPAR-α and PPAR-γ，complanatoside A can increase the expression of ATGL，promote the hydrolysis of liver TG，reduce the deposition of fat in liver，alleviate oxidative stress，inhibit the secretion of TNF-α and IL-6，and relieve inflammation，so as to restore the normal function of hepatocytes. |
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