4-hydroxy-2-nonenal and 3-3--4-5--tetrahydroxystilbene

4-hydroxy-2-nonenal has been researched along with 3-3--4-5--tetrahydroxystilbene* in 1 studies

Other Studies

1 other study(ies) available for 4-hydroxy-2-nonenal and 3-3--4-5--tetrahydroxystilbene

Article	Year
Piceatannol attenuates 4-hydroxynonenal-induced apoptosis of PC12 cells by blocking activation of c-Jun N-terminal kinase. Annals of the New York Academy of Sciences, 2009, Volume: 1171 Alzheimer's disease (AD) is an age-related neurodegenerative disorder in which apoptosis plays a potentially important role. 4-Hydroxynonenal (HNE) is a major lipid peroxidation product produced by oxidative stress, and its level is elevated in the AD brain. In the present study, piceatannol (but not resveratrol) at the concentration of 20 micromol/L inhibited HNE-induced PC12 cell death. Treatment with HNE induced nuclear condensation in PC12 cells, and this was attenuated by piceatannol treatment. HNE induced poly(ADP-ribose) polymerase cleavage and decreased Bcl-2 expression, with both of these effects being attenuated by piceatannol. Piceatannol also inhibited the phosphorylation of c-Jun N-terminal kinase, which is a key regulator of HNE-induced PC12 cell death. These results indicate that piceatannol has therapeutic potential in the prevention of AD. Topics: Aldehydes; Animals; Apoptosis; Blotting, Western; Cell Nucleus; Cell Proliferation; Cross-Linking Reagents; Dose-Response Relationship, Drug; Enzyme Activation; JNK Mitogen-Activated Protein Kinases; Microscopy, Fluorescence; PC12 Cells; Phosphorylation; Poly(ADP-ribose) Polymerases; Proto-Oncogene Proteins c-bcl-2; Rats; Stilbenes	2009

Article

Year

Piceatannol attenuates 4-hydroxynonenal-induced apoptosis of PC12 cells by blocking activation of c-Jun N-terminal kinase.

Annals of the New York Academy of Sciences, 2009, Volume: 1171

Alzheimer's disease (AD) is an age-related neurodegenerative disorder in which apoptosis plays a potentially important role. 4-Hydroxynonenal (HNE) is a major lipid peroxidation product produced by oxidative stress, and its level is elevated in the AD brain. In the present study, piceatannol (but not resveratrol) at the concentration of 20 micromol/L inhibited HNE-induced PC12 cell death. Treatment with HNE induced nuclear condensation in PC12 cells, and this was attenuated by piceatannol treatment. HNE induced poly(ADP-ribose) polymerase cleavage and decreased Bcl-2 expression, with both of these effects being attenuated by piceatannol. Piceatannol also inhibited the phosphorylation of c-Jun N-terminal kinase, which is a key regulator of HNE-induced PC12 cell death. These results indicate that piceatannol has therapeutic potential in the prevention of AD.

Topics: Aldehydes; Animals; Apoptosis; Blotting, Western; Cell Nucleus; Cell Proliferation; Cross-Linking Reagents; Dose-Response Relationship, Drug; Enzyme Activation; JNK Mitogen-Activated Protein Kinases; Microscopy, Fluorescence; PC12 Cells; Phosphorylation; Poly(ADP-ribose) Polymerases; Proto-Oncogene Proteins c-bcl-2; Rats; Stilbenes

2009