Neuroprotective Effects of Methyl 3,4-dihydroxybenzoate Against H₂O₂-Induced Apoptosis in RGC-5 Cells

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  • Zhou Xing
    Department of Pharmacology, School of Medicine, Jinan University, China The Ministry of Basic Medicine, Yichun Vocational and Technical College, China
  • Su Chao-Fen
    Department of Pharmacology, School of Medicine, Jinan University, China
  • Zhang Zheng
    The First Affiliated Hospital of Jinan University, China
  • Wang Chen-Yu
    Department of Clinical Medicine, School of Medicine, Jinan University, China
  • Luo Jin-Qi
    Department of Clinical Medicine, School of Medicine, Jinan University, China
  • Zhou Xiao-Wen
    Pharmacy Department of GuangZhou Chest Hospital, China
  • Cai Liang
    Department of Pharmacology, School of Medicine, Jinan University, China
  • Yan Li
    Department of Pharmacology, School of Medicine, Jinan University, China
  • Zhang Wei
    Department of Pharmacology, School of Medicine, Jinan University, China
  • Luo Huan-Min
    Department of Pharmacology, School of Medicine, Jinan University, China Institute of Brain Sciences, Jinan University, China The Joint Laboratory of Brain Function and Health, Jinan University and The University of Hong Kong, Jinan University, China

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  • Neuroprotective Effects of Methyl 3,4-dihydroxybenzoate Against H<sub>2</sub>O<sub>2</sub>-Induced Apoptosis in RGC-5 Cells

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In the present study, we investigated the protective effect of methyl 3,4-dihydroxybenzoate (MDHB) against H2O2-induced apoptosis in RGC-5 cells. The RGC-5 cells were cultured in plates for 24 h, which were then pretreated with dimethyl sulfoxide, different concentrations of MDHB, or probucol for 12 h prior to addition of 300 μM H2O2 for 24 h. The cell viability was detected by MTT assay. The rate of apoptosis, level of lipid peroxidation, and mitochondrial membrane potential (MMP) were detected by flow cytometry. Western blot analysis was also used to measure the expression level of Bcl-2, Bax, caspase 9, and caspase 3 proteins in H2O2-treated RGC-5 cells. Our study showed that the cell viability of RGC-5 cells significantly decreased after treatment with 300 μM H2O2 for 24 h, but MDHB (8, 16, 32 μM) increased RGC-5 cell survival, suppressed the rate of apoptosis, scavenged reactive oxygen species, and restored MMP. MDHB also obstructed H2O2-induced apoptosis by regulating the expression of Bcl-2 and Bax, as well as suppressing the activation of caspase 9 and caspase 3. Our results showed that MDHB is an effective neuroprotective compound that mitigates oxidative stress and inhibits apoptosis in RGC-5 cells.

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