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CJAP ›› 2016, Vol. 32 ›› Issue (5): 426-430.doi: 10.13459/j.cnki.cjap.2016.05.011

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Effects of exendin-4 on methylglyoxal-induced oxidative stress in PC12 cells

ZHOU Qing1, WANG Yan-ping2,3, LIU Xiao-ying1, LIU Xiao-hong1, PAN Xiao-dong4, CHEN Zhou5, LIU Li-bin1,2,6   

  1. 1. Fujian Institute of Endocrinology, Fuzhou 350001, China;
    2. Department of Endocrinology, Fujian Medical University Union Hospital, Fuzhou 350001, China;
    3. Department of Geriatrics, Fujian Medical University Union Hospital, Fuzhou 350001, China;
    4. Fujian Institute of Geriatrics, Fuzhou 350001, China;
    5. College of Pharmacology, Fujian Medical University, Fuzhou 350001, China;
    6. Academy of Science of Elderly Health, Fujian Medical University, Fuzhou 350001, China
  • Received:2015-08-21 Revised:2016-05-16 Online:2016-09-28 Published:2018-06-20
  • Supported by:
    国家临床重点专科基金(老年医学项目)(2015-GJLN-1-03);福建省临床重点专科基金(内分泌)(2015)

Abstract: Objective: To study whether Exendin-4(Ex-4) could influence oxidative stress in PC12 cells induced by methylglyoxal and its underlying mechanism. Methods: PC12 cells were cultured with methylglyoxal (0,0.25,0.50,0.75,1.0,2.0 mmol/L) for 12~48 h, or PC12 cells were pretreated with Ex-4 (25, 50, 100, 200 nmol/L) for 24 h then incubatedwith methylglyoxal (0.75 mmol/L) for 24 h. MTT assay was used to measure cell viability. Fluorescent probe method was used to detect reactive oxygen species (ROS) expression. Xanthine oxidase method was used to detect superoxide dismutase (SOD)activity. With pretreatment of Exendin-4 (100 nmol/L) for 24 h,the expressions ofP-IκBα, Inhibitor of NF-κB-α IκBα were detected by Western blot after PC12 cells were exposed to methylglyoxal (0.75 mmol/L) for 1 h. Results: Following methylglyoxal administration, cell viability was gradually decreased in a dose-and time-dependent manner. Pretreatment with Ex-4 for 24 hours, cellviability were gradually increased compared with methylglyoxal-alone group. Pretreatment with Ex-4 (100 nmol/L) for 24 hours, ROS expression was reduced by65.30% (P<0.01) compared with methylglyoxal-alone group, ROS expression in NAC-pretreatment group was reduced by 107.40% (P<0.01); SOD activity in the Ex-4 pretreatment group was increased by 5.30 U/mg prot (P<0.01), SOD activity in the NAC pretreatment group was increased by 8.53 U/mg prot (P<0.01);the ratio of P-IκB-α/IκB-α in the Ex-4 pretreatment group was reduced by 25.50% (P<0.01), the ratio of P-IκB-α/IκB-α in the NAC pretreatment group was reduced by 35.14% (P<0.01). Conclusion: This study demonstrates that Ex-4 can increase the viabilities of PC12 cells and protect PC12 cells from oxidative stress induced by methylglyoxal, the mechanism may involve in suppressing the activation of protein IκB-α.

Key words: PC12 cells, methylglyoxal, oxidative stress, Exendin-4, NAC

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