期刊文献+

乳源β-酪啡肽-5对C2C12细胞的抗氧化损伤作用 被引量:2

Protective Effect of β-Casomorphin5 against Oxidative Damage in C2C12 Cells
下载PDF
导出
摘要 通过建立过氧化氢(H2O2)对C2C12细胞的氧化损伤模型,从细胞水平探讨β-酪啡肽-5(β-casomorphin5,β-CM5)对H2O2致氧化应激损伤的保护作用及其可能机制。方法:1)MTT法测定72h内β-CM5对C2C12细胞活力的影响,筛选安全剂量;2)测定不同浓度H2O2对C2C12细胞活力的影响,筛选H2O2的最佳剂量和作用时间;3)测定β-CM5对H2O2损伤后细胞活力的影响;4)检测培养液中超氧化物歧化酶(superoxidedismutase,SOD)、乳酸脱氢酶(lactate dehydrogenase,LDH)的活性。结果:1)β-CM5各浓度组MTT值与对照组无差异;2)0.25mmol/L的H2O2作用于C2C12细胞1h,MTT值显著低于对照组(P<0.01);3)与损伤组相比,β-CM5预保护组的MTT值显著升高(P<0.05),治疗组MTT值无明显变化;4)与损伤组相比,β-CM5预保护组的SOD活性显著提高(P<0.05),LDH活性显著下降(P<0.05)。结论:β-CM5具有较强的抗氧化作用,对H2O2损伤的C2C12细胞有明显的保护作用,其机制可能与增强抗氧化酶活力和维持细胞完整性有关。 Objective: To explore the protective effect and potential mechanism of β-casomorphin5(β-CM5) against hydrogen peroxide(H2O2)-induced oxidative damage in C2C12 cells.Methods: MTT method was used to determine the effect of β-CM5 on cell viability within 72 h and to screen the safe dose.Meanwhile,the effect of H2O2 with various concentrations on cell viability was also evaluated.In addition,the activities of superoxidedismutase(SOD) and lactate dehydrogenase(LDH) in medium were determined.Results: Compared with the control group,the values of MTT in β-CM5 groups with various concentrations did not exhibit an obvious difference.In contrast,a significant decrease in MTT values of C2C12 cells was observed after 1 h of treatment with 0.25 mmol/L H2O2(P 0.01);Compared with the oxidative damage group,MTT value in the β-CM5 pre-protection group was significantly higher(P 0.05),while MTT value in the β-CM5 treatment group had no significant difference when compared to the oxidative damage group.Compared with the oxidative damage group,the activity of SOD in β-CM5 pre-protection group was significantly increased(P 0.05),while the activity of LDH was significantly decreased(P0.05).Conclusion:β-CM5 has a strong antioxidant and pre-protective effect on H2O2-induced damage of C2C12 cells.The mechanism may be related to the increased activity of antioxidant enzymes and maintenance of cell integrality.
出处 《食品科学》 EI CAS CSCD 北大核心 2011年第9期257-260,共4页 Food Science
基金 国家自然科学基金项目(300070565)
关键词 β-酪啡肽-5 C2C12 过氧化氢 超氧化物歧化酶(SOD) 乳酸脱氢酶(LDH) β-casomorphin5 C2C12 cell hydrogen peroxide superoxidedismutase(SOD) lactate dehydrogenase(LDH)
  • 相关文献

参考文献16

  • 1SIMONIAN N A, COYLE J T. Oxidative stress in neurodegenerative diseases[J]. Annu Rev Pharmacol Toxicol, 1996, 36: 83-106. 被引量:1
  • 2FEODMAN E L. Oxidative stress and diabetic neuropathy: a new under- standing of an old problem[J]. J Clinical Investigation, 2003, 111: 431 - 433. 被引量:1
  • 3BROWNLEE M. The pathobiology of diabetic complications: a unify- ing mechanism[J]. Diabetes, 2005, 54(6): 1615-1625. 被引量:1
  • 4NISHIKAWA T, SASAHARA T, KIRITOSHI S, et al. Evaluation of urinary 8-hydroxydeoxy-guaaosine as a novel biomarker of macrovascular complications in type 2 diabetes[J]. Diabetes Care, 2003, 265: 1507- 1512. 被引量:1
  • 5BRANTL V, TESCHEMACHER H, HENSCHEN A, et al. Novel opioid peptides derived from casein (beta-casomorphins). 1. Isolation from bovine casein peptone[J]. Hoppe-Seylers Zeitschrift Fur Physiologische Chemie, 1979, 360: 1211-1216. 被引量:1
  • 6范英兰..β-酪啡肽-5对糖尿病大鼠血糖和氧化应激的影响[D].南京农业大学,2010:
  • 7顾伟,范昕建,吴疆,牛智强.胡黄连苷Ⅱ对H_2O_2损伤L-02细胞的保护作用[J].世界华人消化杂志,2008,16(29):3274-3278. 被引量:25
  • 8戴红良,王洪新,吴国强,王东海.左卡尼汀对心肌细胞H_2O_2损伤的保护作用[J].辽宁医学院学报,2009,30(1):4-6. 被引量:17
  • 9曹艳,许自川,何小解,党西强,易著文,曾雪琪.儿茶素拮抗过氧化氢诱导的大鼠内皮祖细胞凋亡[J].中国当代儿科杂志,2009,11(1):61-64. 被引量:13
  • 10KITAMURA Y, OTA T, MATSUOKA Y, et al. Hydrogen peroxide- induced apoptosis mediated by p53 protein in glialce cells[J]. Glia, 1999. 25(2): 154-164. 被引量:1

二级参考文献45

共引文献81

同被引文献38

  • 1CONNOR M K, IRRCHER I, HOOD D A. Contractile activityinduced transcriptional activation of cytochrome c involves spl and is proportional to mitochondria ATP synthesis in C2C12 muscle cells[J]. J Biol Chem, 2001,276 (19) : 15898-15904. 被引量:1
  • 2FROSIG C, JORGENSEN S B, HARDIE DG, et al. 5 '-AMP- activated protein kinase activity and protein expression are regulated by endurance training in human skeletal muscle [J]. Am J Physiol Endocrinol Metab, 2004,286 (3):411-417. 被引量:1
  • 3FUJIMOTO E, MACHIDA S, HIGUCHI M, et al. Effects of nonexhaustive bouts of high intensity intermittent swimming training on GLUT-4 expression in rat skeletal muscle [J]. Physiol Sci, 2010,60 (2):95-101. 被引量:1
  • 4JENSEN T E, RICHTER E A. Regulation of glucose and glycogen metabolism during and after exercise [J]. J Physiol, 2012,590:1069-1076. 被引量:1
  • 5JORGENSEN S B, TRCCBAK J T, VIOLLCT B, et al. Role of AMPK-α2 in basal,training,and AICAR-induced GLUT4 hexokinase and mitochondrial protein expression in mouse muscle[J]. Am J Physiol Endoerinol Mctab, 2007,292 (1): 331-339. 被引量:1
  • 6KARLSSON H K, CHIBALIN A V,KOISTINEN H A, etal. Kinetics of GLUT4 trafficking in rat and human skeletal muscle[J]. Diabetes , 2009,58 : 847-854. 被引量:1
  • 7LAURITZEN H P, GALBO H, TOYODA T, et al. Kinetics of Contraction-induced GLUT4 translocation in skeletal muscle fibers from living mice[J]. Diabetes, 2010,59 : 2134-2144. 被引量:1
  • 8LEE-YOUNG R S,GRIFFEE SR, LYNES S E. Skeletal muscle AMP-activated protein kinase Is essential for the metabolic response to exereisee in vivo[J]. J Biol Chem, 2009,284, 23925- 23934. 被引量:1
  • 9MAARBJERG S J, JORGENSEN S B, ROSE A J, et al. Genetic impairment of AMPK-α2 signaling does not reduce muscle glucose uptake during treadmill exercise in mice[J]. Am J Physiol Endocrinol Metab, 2009,297(4) : 924-934. 被引量:1
  • 10MAROTTA M, BRAGOS R, GOMEZ-FOIX A M. Design and perfor-mance of an electrical stimulator for long-term contraction of cultured muscle cells[J]. Biotechniques, 2004,36 (1) : 68- 73. 被引量:1

引证文献2

二级引证文献5

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部