期刊
JOURNAL OF HUAZHONG UNIVERSITY OF SCIENCE AND TECHNOLOGY-MEDICAL SCIENCES
卷 32, 期 5, 页码 737-745出版社
SPRINGER
DOI: 10.1007/s11596-012-1027-1
关键词
1,2,3,4,6-penta-O-galloyl-beta-D-glucose (beta-PGG); heme oxygenase-1; oxidative stress; NF-E2-related factor2; ERK1/2; Akt; Parkinson's disease
资金
- National 11th Five-Year Plan Research Foundation of China [2006BAI01A14]
This study examined the ability of 1,2,3,4,6-penta-O-galloyl-beta-D-glucose (beta-PGG) to induce the expression of heme oxygenase-1 (HO-1) in the PC12 cells and its regulation in the PC12 cells. One week before treatment with the drug, nerve growth factor (NGF) was added to the cultures at a final concentration of 50 ng/mL to induce neuronal differentiation. After drug treatment, HO-1 gene transcription was analyzed by reverse transcription polymerase chain reaction (RT-PCR). Expression of HO-1 and NF-E2-related factor2 (Nrf2) and activation of extracellular signal-regulated kinase (ERK) and Akt were detected by Western blotting. The viability of the PC12 cells treated with different medicines was examined by MTT assay. The oxidative stress in the PC12 cells was evaluated qualitatively and quantitatively by DCFH-DA. The results showed that beta-PGG up-regulated HO-1 expression and this increased expression provided neuroprotection against MPP+-induced oxidative injury. Moreover, beta-PGG induced Nrf2 nuclear translocation, which was found to be upstream of beta-PGG-induced HO-1 expression, and the activation of ERK and Akt, a pathway that is involved in beta-PGG-induced Nrf2 nuclear translocation, HO-1 expression and neuroprotection. In conclusion, beta-PGG up-regulates HO-1 expression by stimulating Nrf2 nuclear translocation in an ERK- and Akt-dependent manner, and HO-1 expression by beta-PGG may provide the PC12 cells with an acquired antioxidant defense capacity to survive the oxidative stress.
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