期刊
BIOLOGICAL & PHARMACEUTICAL BULLETIN
卷 33, 期 11, 页码 1841-1846出版社
PHARMACEUTICAL SOC JAPAN
DOI: 10.1248/bpb.33.1841
关键词
geniposide; heme oxygenase-1; nuclear factor-E2-related factor 2; oxidative stress
资金
- National Natural Science Foundation of China [30701020]
- Program for New Century Excellent Talents in University [NCET-07-0913]
- Chongqing Science and Technology Commission (CSTC) [2007AA5029]
- Chongqing Municipal Education Committee [KJ0707009]
Oxidative stress in brain is emerging as a potential causal factor in aging and age-related neurodegenerative disorders. A large body of evidence shows that induction of endogenous antioxidative proteins seems to be a reasonable strategy for delaying the progression of cell injury. En this study, geniposide upregulates the expression of heme oxygenase-1 (HO-1) to attenuate the cell apoptosis induced by 3-morpholinosydnonimine hydrochloride (SIN-1) in primary cultured hippocampal neurons. Furthermore, geniposide induces the nuclear translocation of nuclear factor-E2-related factor 2 (Nrf2) and activation of phosphatidylinositol 3'-kinase (PI3K) in the presence of oxidative stress, and both LY294002 (a specific inhibitor of PI3K) and Zinc protoporphyrin (ZnPP, an inhibitor of HO-1) decrease the cytoprotective action of geniposide in hippocampal neurons. Taken together, the novel cytoprotective mechanism of geniposide to antagonize oxidative stress may be involved in PI3K- and Nrf2-mediated upregulation of the antioxidative enzyme HO-1.
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