林天南博士
兼任研究員
- 886-2-2789-9141 (Lab) (Room No: 404)
- 2652-3936 (Office)
- 2785-8847 (Fax)
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Specialty:
- Cerebral Ischemia
- Angiogenesis
- Neurochemistry
Education and Positions:
Ph.D. in Biochemistry, Univ. of Missouri-Columbia.
Highlight Detail
15-Deoxy-∆12,14-PGJ 2, by Activating Peroxisome Proliferator-Activated Receptor-Gamma, Suppresses p22phox Transcription to Protect Brain Endothelial Cells Against Hypoxia-Induced Apoptosis.
Dr. Lin, Teng-Nan
Mol Neurobiol., Dec 19, 201315-Deoxy-∆12,14-PGJ2 (15d-PGJ2) and thiazolidinedione attenuate reactive oxygen species (ROS) production via a peroxisome proliferator-activated receptor-gamma (PPAR-γ)-dependent pathway. Nonetheless, how PPAR-γ mediates ROS production to ameliorate ischemic brain injury is not clear. Recent studies indicated that nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is the major source of ROS in the vascular system. In the present study, we used an in vitro oxygen-glucose deprivation and reoxygenation (hypoxia reoxygenation [HR]) paradigm to study whether PPAR-γ interacts with NADPH oxidase, thereby regulating ROS formation in cerebral endothelial cells (CECs).