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作 者:郭勇 秦汉雄 魏贞 方丽 闵伟红 GUO Yong;QIN Hanxiong;WEI Zhen;FANG Li;MIN Weihong(National Engineering Laboratory on Wheat and Corn Further Processing,College of Food Science and Engineering,Jilin Agricultural University,Changchun 130118,China)
机构地区:[1]吉林农业大学食品科学与工程学院小麦和玉米深加工国家工程实验室
出 处:《食品科学》2019年第13期143-149,共7页Food Science
基 金:国家高技术研究发展计划(863计划)项目(2013AA102206)
摘 要:通过细胞实验和NF-κB/iNOS/NO信号通路研究长白山核桃源五肽Leu-Pro-Leu-Leu-Arg(LPLLR)对过氧化氢诱导氧化损伤的PC12细胞保护作用的机制。结果显示:LPLLR对PC12细胞无毒副作用,能显著提高受氧化损伤PC12细胞的存活率,降低细胞中活性氧和丙二醛含量,提高超氧化物歧化酶(superoxide dismutase,SOD)、过氧化氢酶、谷胱甘肽过氧化物酶活力和乙酰胆碱含量(P<0.05,P<0.001)。通过酶联免疫吸附检测法和Western blotting法检测NO分泌量和SOD2、核转录因子κB(nuclear transcription factor-κB,NF-κB)p65、诱导型一氧化氮合酶(inducible nitricoxide synthase,iNOS)蛋白表达水平,发现LPLLR能显著降低NO分泌量并上调SOD2蛋白表达水平,下调NF-κB p65和iNOS蛋白表达水平(P<0.05,P<0.001)。表明LPLLR对氧化应激损伤的PC12细胞具有一定的保护作用。The protective effect of the pentapeptide Leu-Pro-Leu-Leu-Arg (LPLLR) from manchurian walnut (Juglans mandshurica Maxim) meal protein on PC12 cells against hydrogen peroxide (H2O2)-induced damage were investigated and the underlying mechanism was elucidated based on the NF-κB/iNOS/NO signaling pathway. The results showed that LPLLR had no cytotoxicity and significantly increased the survival rate of PC12 cells suffering from oxidative stress induced by H2O2. LPLLR could reduce the production of reactive oxygen species (ROS) and malondialdehyde (MDA), and enhance the activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) and acetylcholine (ACh) level (P < 0.05, P < 0.001) in H2O2-induced PC12 cells. ELISA and Western blotting results confirmed that LPLLR could up-regulate the expression of SOD2 and down-regulate the expression of nuclear transcription factor-κB (NF-κB) p65 and inducible nitricoxide synthase (iNOS), as well as decrease the secretion of NO (P < 0.05, P < 0.001). Therefore, LPLLR can protect PC12 cells against hydrogen peroxide-induced injury.
分 类 号:TS209[轻工技术与工程—食品科学]
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