Abstract | BACKGROUND: METHODS: RESULTS: LPE pretreatment conferred significant protection against the H2O2-induced decrease of SH-SY5Y cell viability. H2O2-induced increases of intracellular oxidative stress and mitochondrial dysfunction were attenuated by LPE pretreatment. Therefore, LPE pretreatment prevented SH-SY5Y cell injury. Treatment with H2O2 significantly induced poly(ADP ribose) polymerase (PARP) and caspase-3 cleavage, which was blocked by LPE. We found that p38 activation was involved in the neuroprotective effects of LPE. CONCLUSIONS: Current findings suggest that LPE exerts neuroprotective effects against H2O2-induced apoptotic cell death by modulating p38 activation in SH-SY5Y cells. Therefore, LPE has potential anti-apoptotic effects that may be neuroprotective in neurodegenerative diseases and aging-related dementia.
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Authors | Hee Ra Park, Heeeun Lee, Hwayong Park, Jong Wook Jeon, Won-Kyung Cho, Jin Yeul Ma |
Journal | BMC complementary and alternative medicine
(BMC Complement Altern Med)
Vol. 15
Pg. 171
(Jun 09 2015)
ISSN: 1472-6882 [Electronic] England |
PMID | 26054856
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antioxidants
- Neuroprotective Agents
- Plant Extracts
- Hydrogen Peroxide
- Poly(ADP-ribose) Polymerases
- Caspase 3
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Topics |
- Antioxidants
(pharmacology)
- Apoptosis
(drug effects)
- Caspase 3
(metabolism)
- Cell Death
(drug effects)
- Cell Line, Tumor
- Cell Survival
(drug effects)
- Dementia
(drug therapy, metabolism)
- Humans
- Hydrogen Peroxide
(metabolism)
- Liliaceae
- Membrane Potential, Mitochondrial
(drug effects)
- Mitochondria
(drug effects)
- Neuroblastoma
(metabolism)
- Neurodegenerative Diseases
(drug therapy, metabolism)
- Neurons
(drug effects, metabolism)
- Neuroprotective Agents
(pharmacology)
- Oxidative Stress
(drug effects)
- Phytotherapy
- Plant Extracts
(pharmacology)
- Poly(ADP-ribose) Polymerases
(metabolism)
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