發(fā)布時間：2018-04-20 01:14

  本文選題：棕櫚酸 + NADPH氧化酶　； 參考：《南方醫(yī)科大學學報》2016年05期

【摘要】：目的觀察棕櫚酸(PA)對肝細胞氧化應激反應及炎癥小體產生的影響。方法(1)將正常小鼠肝細胞AML12分別用不同濃度的棕櫚酸(0、0.15、0.25、0.4 mmol/L)處理;(2)將AML12細胞分為空白對照組(control組)、棕櫚酸組(PA組)及棕櫚酸+N-乙酰半胱氨酸組(PA+NAC組)并予以相應藥物處理。24 h后檢測細胞中脂肪沉積情況、細胞總ROS、線粒體來源ROS、NOX4蛋白表達、NOX4的定位以及炎癥小體和IL-1β的表達。結果與control組相比,PA組細胞質中脂滴增加,細胞總ROS(12463.09±2.72 vs 6691.23±2.45,P=0.00)及線粒體來源ROS含量(64.98±0.94 vs 45.04±0.92,P=0.00)上升,NOX4、NLRP3、ASC、caspase-1蛋白表達增加,IL-1β表達增加(1603.52±1.32 vs 2629.33±2.57,P=0.00),且發(fā)現線粒體和NOX4在細胞質中存在共定位,而抗氧化劑NAC除了能使PA誘導的ROS產生減少(7782.15±2.87 vs 5445.6±1.17,P=0.00),還可使NLRP3、ASC及caspase-1蛋白表達下降。結論棕櫚酸刺激肝細胞后,可以導致脂滴在肝細胞質中大量沉積,亦可以通過線粒體和NOX4途徑導致肝細胞氧化應激反應,并因此促進細胞炎癥小體的激活和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 鹵2.72 vs 6691.23 鹵2.45 P0. 00) and mitochondrial ROS content increased 64.98 鹵0.94 vs 45.04 鹵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 鹵1.32 vs 2629.33 鹵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 鹵2.87) vs 5445.6 鹵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.
【作者單位】： 南方醫(yī)科大學南方醫(yī)院消化科;
【基金】：國家自然科學基金(81470844) 廣州市臨床醫(yī)學研究與轉化中心(胃腸道早期腫瘤)試點建設項目(741569196402)~~
【分類號】：R965

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