|
|
|
| Effects of high glucose state on oxidative stress in prostate cancer cells |
| ZHANG Zhitao1 ZHANG Hongyan2 NIU Fangfang1 |
1.The Second Department of Uropoiesis Surgical, Handan Central Hospital, Hebei Province, Handan 056001, China;
2.Department of Inspection, Medical College of Hebei Engineering University , Hebei Province, Handan 056001, China |
|
|
|
Abstract Objective To explore the effects of high glucose state on oxidative stress in prostate cancer cells. Methods Human prostate cancer cell line LNCap was treated with different glucose concentrations, and the level of LNCap cells reactive oxygen species (ROS) was detected by DCFH-DA fluorescent probe. The hydrogen peroxide (H2O2), total superoxide dismutase (T-SOD), catalase (CAT) and glutathione peroxidase (GPX) kits were used to detect H2O2 level and antioxidant enzymes activities in LNCap cells. Western blot was used to detect the expression levels of SOD1 and SOD2 protein in LNCap cells. The level of H2O2 was detected after LNCap cells transfected with si-SOD2. Results The levels of ROS and H2O2 in LNCap cells were increased with the increase of glucose concentration, and were concentration-dependent (P < 0.05). The activities of T-SOD and CAT in LNCap cells were increased significantly in the high glucose environment (P < 0.05), but there was no significant change in the activity of GPX (P > 0.05). In the high glucose environment, the expression level of SOD2 in LNCap cells was increased significantly (P < 0.05), but the expression level of SOD1 was not significantly changed (P > 0.05). After the SOD2 gene was silenced, the level of H2O2 in the LNCap cells was decreased significantly in the high glucose environment (P < 0.05). Conclusion High glucose state can promote the oxidative stress level of prostate cancer cells, and the increase of H2O2 level may be regulated by the expression of SOD2.
|
|
|
|
|
|
[1] 叶定伟，朱耀.中国前列腺癌的流行病学概述和启示[J].中华外科杂志，2015，53（4）：249-252.
[2] 曾胜，岳亮，申慧青，等.糖尿病对前列腺癌的影响[J].现代泌尿外科杂志，2016，21（7）：558-561.
[3] 郑岚，钟春生，郑浩，等.2型糖尿病与恶性肿瘤关系的临床回顾性研究[J].安徽中医药大学学报，2015，34（3）：40-41.
[4] 王许，李庆龙，刘颖.2型糖尿病与肺癌发生的相关性分析[J].癌症进展，2016，14（7）：693-695.
[5] 高梅娟，张丽杰，于春梅.抗糖尿病药物与乳腺癌相关性研究[J].中国预防医学杂志，2016，17（6）：442-446.
[6] 姜新，吕然然，谢晓娜，等.糖尿病与胰腺癌关系的研究进展[J].中国实验诊断学，2016，20（2）：338-339.
[7] 王欢，赵晓梅，杨倩.糖尿病与膀胱癌关系的病例对照研究[J].哈尔滨医科大学学报，2015，49（4）：335-337.
[8] 许召杰，周学良，豆萌萌，等.降糖药物与2型糖尿病患者大肠癌发病风险及疗效的Meta分析[J].中华普通外科杂志，2016，31（7）：596-600.
[9] 姚志灵，陈亮，王欣丽.不同糖代谢状态冠心病患者氧化应激的研究进展[J].中国医药导报，2015，12（26）：46-49.
[10] Geybels MS，Pa VDB，van Schooten FJ，et al. Oxidative stress-related genetic variants，pro-and antioxidant intake and status，and advanced prostate cancer risk [J]. Cancer Epidemiol Biomarkers Prev，2015，24（1）：178-186.
[11] Giovannucci E，Harlan DM，Archer MC，et al. Diabetes and cancer：a consensus report [J]. CA Cancer J Clin，2010， 60（4）：207-221.
[12] Atchison EA，Gridley G，Carreon JD，et al. Risk of cancer in a large cohort of U.S. veterans with diabetes [J]. Int J Cancer，2011，128（3）：635643.
[13] Wang M，Hu RY，Wu HB，et al. Cancer risk among patients with type 2 diabetes mellitus：a population-based prospective study in China [J]. Sci Rep，2015，2016，5：11 503.
[14] Long XJ，Lin S，Sun YN，et al. Diabetes mellitus and prostate cancer risk in Asian countries：a meta-analysis [J]. Asian Pac J Cancer Prev，2012，13（8）：4097-4100.
[15] 张志涛，张红艳.氧化应激在良性前列腺增生和前列腺癌发病中的作用研究[J].现代预防医学，2013，40（9）：1781-1782.
[16] 梁馨予，张婷，周永，等.杨梅素减轻高糖诱导的血管内皮细胞氧化应激损伤[J].第三军医大学学报，2013，35（21）：2301-2305.
[17] Jin Y，Wang L，Qu S，et al. STAMP2 increases oxidative stress and is critical for prostate cancer [J]. EMBO Mol Med，2015，7（3）：315-331.
[18] Li W，Ma Q，Liu J，et al. Hyperglycemia as a mechanism of pancreatic cancer metastasis [J]. Front Biosci，2012， 17（1）：1761-1774.
[19] 黎韡，徐勤鸿，马清涌.高糖状态对胰腺癌细胞氧化应激水平的促进作用[J].西安交通大学学报：医学版，2016， 37（6）：789-794.
[20] 王悦，徐开红，徐萍.氧化应激反应因子CAT、GPX1、SOD1、SOD2、TXNL1和LOX-1与反复自然流产的相关性[J].中国卫生检验杂志，2014，24（17）：2515-2517. |
|
|
|
