棕榈酸通过肝细胞氧化应激反应激活炎症小体
发布时间:2018-04-20 01:14
本文选题:棕榈酸 + NADPH氧化酶 ; 参考:《南方医科大学学报》2016年05期
【摘要】:目的观察棕榈酸(PA)对肝细胞氧化应激反应及炎症小体产生的影响。方法(1)将正常小鼠肝细胞AML12分别用不同浓度的棕榈酸(0、0.15、0.25、0.4 mmol/L)处理;(2)将AML12细胞分为空白对照组(control组)、棕榈酸组(PA组)及棕榈酸+N-乙酰半胱氨酸组(PA+NAC组)并予以相应药物处理。24 h后检测细胞中脂肪沉积情况、细胞总ROS、线粒体来源ROS、NOX4蛋白表达、NOX4的定位以及炎症小体和IL-1β的表达。结果与control组相比,PA组细胞质中脂滴增加,细胞总ROS(12463.09±2.72 vs 6691.23±2.45,P=0.00)及线粒体来源ROS含量(64.98±0.94 vs 45.04±0.92,P=0.00)上升,NOX4、NLRP3、ASC、caspase-1蛋白表达增加,IL-1β表达增加(1603.52±1.32 vs 2629.33±2.57,P=0.00),且发现线粒体和NOX4在细胞质中存在共定位,而抗氧化剂NAC除了能使PA诱导的ROS产生减少(7782.15±2.87 vs 5445.6±1.17,P=0.00),还可使NLRP3、ASC及caspase-1蛋白表达下降。结论棕榈酸刺激肝细胞后,可以导致脂滴在肝细胞质中大量沉积,亦可以通过线粒体和NOX4途径导致肝细胞氧化应激反应,并因此促进细胞炎症小体的激活和IL-1β的分泌。
[Abstract]:Objective to observe the effects of palmitic acid (PAA) on oxidative stress and inflammatory corpuscles in hepatocytes. Methods 1) AML12 of normal mouse hepatocytes was treated with different concentrations of 0. 15mmol / L palmitate 0.250.25nmol / L) AML12 cells were divided into control group (control group), palmitic acid group (PA group) and palmitic acid group (nacetylcysteine group (NAC group)). Lipid deposition in cells should be detected after drug treatment for 24 hours. The localization of NOX4 protein and the expression of inflammatory corpuscles and IL-1 尾. Results compared with control group, lipid droplets in cytoplasm of PA group increased, total ROS(12463.09 卤2.72 vs 6691.23 卤2.45 P0. 00) and mitochondrial ROS content increased 64.98 卤0.94 vs 45.04 卤0.92P0. 00. the expression of NLRP3Ascaspase-1 protein was increased in PA group. The expression of IL-1 尾 was increased by 1603.52 卤1.32 vs 2629.33 卤2.57 P0.000.The co-localization of mitochondria and NOX4 in cytoplasm was also found. The antioxidant NAC not only decreased the ROS production induced by PA (7782.15 卤2.87) vs 5445.6 卤1.17 (P0. 00G), but also decreased the expression of caspase-1 and ASC protein. Conclusion after palmitic acid stimulation, lipid droplets are deposited in the liver cytoplasm, and oxidative stress is induced by mitochondria and NOX4 pathway, thus promoting the activation of inflammatory corpuscles and the secretion of IL-1 尾.
【作者单位】: 南方医科大学南方医院消化科;
【基金】:国家自然科学基金(81470844) 广州市临床医学研究与转化中心(胃肠道早期肿瘤)试点建设项目(741569196402)~~
【分类号】:R965
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