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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Ge, Pengfei Feng, Chunsheng Luo, Tianfei Zhang, Yanhong Luo, Yinan Liu, Kai Zhang, Shuyan |
| Description | Author Affiliation: Feng C ( Department of Anesthesiology, First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.); Luo T ( Department of Neurology, First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.); Zhang S ( Department of Neurosurgery, First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.); Liu K ( Department of Neurosurgery, First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.); Zhang Y ( Department of Emergent Medicine, People's Hospital of Jilin Province, Changchun, Jilin 130021, P.R. China.); Luo Y ( Department of Neurosurgery, First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.); Ge P ( Department of Neurosurgery, First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.) |
| Abstract | Oxidative stress, which is characterized by excessive production of reactive oxygen species (ROS), is a common pathway that results in neuronal injury or death due to various types of pathological stress. Although lycopene has been identified as a potent antioxidant, its effect on hydrogen peroxide (H2O2)induced neuronal damage remains unclear. In the present study, pretreatment with lycopene was observed to protect SHSY5Y neuroblastoma cells against H2O2induced death via inhibition of apoptosis resulting from activation of caspase3 and translocation of apoptosis inducing factor (AIF) to the nucleus. Furthermore, the overproduced ROS, as well as the reduced activities of antioxidative enzymes, superoxide dismutase and catalase, were demonstrated to be alleviated by lycopene. Additionally, lycopene counteracted H2O2induced mitochondrial dysfunction, which was evidenced by suppression of mitochondrial permeability transition pore opening, attenuation of the decline of the mitochondrial membrane potential, and inhibition of the increase of Bax and decrease of Bcl2 levels within the mitochondria. The release of cytochrome c and AIF from the mitochondria was also reduced. These results indicate that lycopene is a potent neuroprotectant against apoptosis, oxidative stress and mitochondrial dysfunction, and could be administered to prevent neuronal injury or death. |
| ISSN | 17912997 |
| e-ISSN | 17913004 |
| DOI | 10.3892/mmr.2016.5056 |
| Journal | Molecular Medicine Reports |
| Issue Number | 5 |
| Volume Number | 13 |
| Language | English |
| Publisher | Spandidos Publications |
| Publisher Date | 2016-05-01 |
| Publisher Place | Greece |
| Access Restriction | Open |
| Subject Keyword | Discipline Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology |
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