淬灭胃癌SGC-7901细胞内活性氧对维生素E琥珀酸脂诱导内质网应激的影响

doi:10.3969/j.issn.1004-616x.2018.04.005

癌变·畸变·突变 ›› 2018, Vol. 30 ›› Issue (4): 270-274.doi: 10.3969/j.issn.1004-616x.2018.04.005

淬灭胃癌SGC-7901细胞内活性氧对维生素E琥珀酸脂诱导内质网应激的影响

黄晓莉¹, 吴坤², 赵莎莎¹

1. 山东大学齐鲁医院营养科, 山东济南 250012;
2. 哈尔滨医科大学营养与食品卫生教研室, 黑龙江哈尔滨 150081

收稿日期:2017-11-08 修回日期:2017-12-26 出版日期:2018-07-30 发布日期:2018-07-30
作者简介:黄晓莉,E-mail:hxl0251010@163.com
基金资助:
国家自然科学基金资助项目（81402663）

Reactive oxygen species scavenging on vitamin E succinate-induced endoplasmic reticulum stress response in SGC-7901 cells

HUANG Xiaoli¹, WU Kun², ZHAO Shasha¹

1. Department of Nutrition, Qilu Hospital of Shandong University, Jinan 250012, Shandong;
2. Department of Nutrition and Food Hygiene, Harbin Medical University, Harbin 150081, Heilongjiang, China

Received:2017-11-08 Revised:2017-12-26 Online:2018-07-30 Published:2018-07-30

摘要/Abstract

摘要： 目的：探讨淬灭胃癌SGC-7901细胞内活性氧（ROS）对维生素E琥珀酸脂（VES）诱导内质网应激的影响。方法：将不同浓度（1、5、10和20 mmol/L）N-乙酰半胱氨酸（NAC）作用胃癌SGC-7901细胞2 h，再加入20 μg/mL VES处理12 h，经2，7-二氢二氯荧光黄双乙酸钠（DCFH-DA）染色后，采用激光共聚焦显微镜观察细胞内ROS水平。另将20 mmol/L NAC作用SGC-7901细胞2 h，再加入20 μg/mL VES处理细胞12 h，经DCFH-DA染色后，流式细胞术进一步检测细胞内ROS水平。将20 mmol/L NAC作用SGC-7901细胞2 h，再加入20 μg/mL VES分别处理15和24 h后，分别采用逆转录PCR（RT-PCR）和Western blotting法检测内质网应激相关分子葡萄糖调节蛋白GRP78和CHOP mRNA及蛋白的表达。结果：与单纯VES处理组相比，20 mmol/L NAC预处理组胃癌细胞内ROS下降最为明显（P < 0.05）。与对照组相比，20 μg/mL VES能够诱导胃癌细胞内GRP78和CHOP mRNA及蛋白的表达明显增加（P < 0.05）；而与单纯20 μg/mL VES处理组相比，20 mmol/L NAC对VES诱导GRP78和CHOP mRNA及蛋白表达具有显著的抑制作用（P < 0.05）。结论：在体外，淬灭胃癌细胞内ROS能够抑制VES诱导的内质网应激反应。

关键词: 活性氧, 维生素E琥珀酸脂, 内质网应激, 胃癌细胞

Abstract: OBJECTIVE: To investigate effects of reactive oxygen species (ROS) scavenging on vitamin E succinate(VES)-induced endoplasmic reticulum stress response (ERS) in human gastric cancer SGC-7901 cells. MATERIALS: SGC-7901 human gastric cancer cells were treated with 1,5,10,20 mmol/L N-acetyl-L-cysteine (NAC) for 2 h and then with 20 μg/mL VES for an additional 12 h;ROS production was measured using confocal microscopy. In addition,cells were pretreated with 20 mmol/L NAC for 2 h and then with 20 μg/mL VES for an additional 12 h;there after,ROS production was measured using flow cytometry. In addition,cells were pretreated with 20 mmol/L NAC for 2 h and subsequently treated with 20 μg/mL VES for 15 h and 24 h,CHOP and GRP78 were determined by RT-PCR and Western blot. RESULTS: Pretreatment with NAC drastically decreased VES-induced ROS generation in SGC-7901 cells (P < 0.05). NAC significantly inhibited induction of CHOP and GRP78 mRNA and protein expression in VES-treated SGC-7901 cells (P < 0.05). CONCLUSION: ER stress response is an event downstream of the oxidative stress induced by VES in SGC-7901 cells.

Key words: reactive oxygen species, vitamin E succinate, endoplasmic reticulum stress, gastric cancer cells

中图分类号:

R730.231

黄晓莉, 吴坤, 赵莎莎. 淬灭胃癌SGC-7901细胞内活性氧对维生素E琥珀酸脂诱导内质网应激的影响[J]. 癌变·畸变·突变, 2018, 30(4): 270-274.

HUANG Xiaoli, WU Kun, ZHAO Shasha. Reactive oxygen species scavenging on vitamin E succinate-induced endoplasmic reticulum stress response in SGC-7901 cells[J]. Carcinogenesis, Teratogenesis & Mutagenesis, 2018, 30(4): 270-274.

参考文献

[1] ZHAO Y,ZHAO X,YANG B,et al. Alpha-tocopheryl succinate-induced apoptosis in human gastric cancer cells is modulated by ERK1/2 and c-Jun N-terminal kinase in a biphasic manner[J]. Cancer Lett,2007,247(2):345-352.
[2] ZHAO Y,LI R,XIA W,et al. Bid integrates intrinsic and extrinsic signaling in apoptosis induced by alpha-tocopheryl succinate in human gastric carcinoma cells[J]. Cancer Lett,2010(1),288(1):42-49.
[3] JIA L,HUANG X L,ZHAO Y,et al. Vitamin E succinate (VES) inhibits cell growth and induces apoptosis by mitochondrial-derived ROS in SGC-7901 cells[J]. Med Sci Monit,2010,16(5):131-139.
[4] YIN ZEYUAN,ZHAO XUE,YANG DAN,et al. LFG-500,a newly synthesized flavonoid,induces apoptosis in human ovarian carcinoma SKOV3 cells with involvement of the reactive oxygen species-mitochondria pathway[J]. Exp Ther Med,2017,13(6):2819-2827.
[5] THANET S,WILAWAN M,YUKIO N,et al. Goniothalamin induces mitochondria-mediated apoptosis associated with endoplasmic reticulum stress-induced activation of JNK in HeLa cells[J]. Oncol Lett,2017,13(1):119-128.
[6] 黄晓莉,赵艳,张志宏,等. 维生素E琥珀酸酯通过内质网应激诱导胃癌SGC-7901细胞凋亡的研究[J]. 癌变·畸变·突变,2012,24(3):195-198.
[7] 黄晓莉,吴坤,赵莎莎. 维生素E琥珀酸脂诱导人胃癌细胞发生未折叠蛋白反应的研究[J]. 癌变·畸变·突变,2017,29(4):256-259.
[8] BREZNICEANU M L,LAU C J,GODIN N,et al. Reactive oxygen species promote caspase-12 expression and tubular apoptosis in diabetic nephropathy[J]. J Am Soc Nephrol,2010,21(6):943-954.
[9] LAMPIASI N,AZZOLINA A,D'ALESSANDRO N,et al. Antitumor effects of dehydroxymethylepoxyquinomicin,a novel nuclear factor-kappaB inhibitor,in human liver cancer cells are mediated through a reactive oxygen species-dependent mechanism[J]. Mol Pharmacol,2009,76(2):290-300.
[10] GUAN L,HAN B,LI Z,et al. Sodium selenite induces apoptosis by ROS-mediated endoplasmic reticulum stress and mitochondrial dysfunction in human acute promyelocytic leukemia NB4 cells[J]. Apoptosis,2009,14(2):218-225.
[11] MOORADIAN A D,HAAS M J. Glucose-induced endoplasmic reticulum stress is independent of oxidative stress:A mechanistic explanation for the failure of antioxidant therapy in diabetes[J]. Free Radic Biol Med,2011,50(9):1140-1143.
[12] PIERACHILLE S,ANGELO C,PAOLO S,et al. Oxidative stress and respiratory system:pharmacological and clinical reappraisal of N-acetylcysteine[J]. COPD,2014,11(6):705-717.
[13] COOK K L,SOTO-PANTOJA D R,CLARKE P A G,et al. Endoplasmic reticulum stress protein GRP78 modulates lipid metabolism to control drug sensitivity and anti-tumor immunity in breast cancer[J]. Cancer Res,2016,76(19):5657-5670.
[14] KIM H,SHAHIN H,KOMUDI S,et al. Parkin regulation of CHOP modulates susceptibility to cardiac endoplasmic reticulum stress[J]. Sci Rep,2017,7:2093.
[15] KADARA H,LACROIX L,LOTAN D,et al. Induction of endoplasmic reticulum stress by the pro-apoptotic retinoid N-(4-hydroxyphenyl)retinamide via a reactive oxygen species-dependent mechanism in human head and neck cancer cells[J]. Cancer Biol Ther,2007,6(5):705-711.
[16] LEE Y J,SUH H N,HAN H J. Effect of BSA-induced ER stress on SGLT protein expression levels and alpha-MG uptake in renal proximal tubule cells[J]. Am J Physiol Renal Physiol,2009,296(6):F1405-1416.
[17] SHEIKH-ALI M,SULTAN S,ALAMIR A R,et al. Effects of antioxidants on glucose-induced oxidative stress and endoplasmic reticulum stress in endothelial cells[J]. Diabetes Res Clin Pract,2010,87(2):161-166.

淬灭胃癌SGC-7901细胞内活性氧对维生素E琥珀酸脂诱导内质网应激的影响

Reactive oxygen species scavenging on vitamin E succinate-induced endoplasmic reticulum stress response in SGC-7901 cells

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