1. Suppression of GRASP65 phosphorylation by tetrahydrocurcumin protects against cerebral ischemia/reperfusion injury via ERK signaling.
- Author
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BIN LIN, HENG YU, YUTING LIN, CHAO CAI, HUOQUAN LU, and XINBO ZHU
- Subjects
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IMMUNOSUPPRESSION , *PHOSPHORYLATION , *TREATMENT of reperfusion injuries , *CELLULAR signal transduction , *LABORATORY mice ,CEREBRAL ischemia treatment - Abstract
The aim of the present study was to assess the neuroprotective effects of tetrahydrocurcumin (THC) in a mouse model of cerebral ischemia/reperfusion (I/R) injury, and to investigate the involvement of Golgi reassembly and stacking protein 65 (GRASP65) and the extracellular signal-regulated kinase (ERK) signaling pathway. Cerebral I/R injury was induced using the Pulsinelli four-vessel occlusion method. After 5 min of reperfusion, mice received THC (5, 10 or 25 mg/kg) or saline by intraperitoneal injection. After 24 h of reperfusion, mice underwent neurological evaluation. Infarct volumes were determined by triphenyltetrazolium chloride staining, and levels of superoxide dismutase and malondialdehyde were measured in brain tissue homogenates. Expression of GRASP65, phosphorylated-GRASP65, ERK and phosphorylated-ERK was determined by western blotting. THC induced a dose-dependent decrease in the phosphorylation of ERK and GRASP65. Thus, THC attenuated I/R injury-induced activation of the ERK signaling pathway and reduced the phosphorylation of GRASP65. THC exhibited a dose-dependent protective effect against cerebral I/R injury, mediated by suppression of the ERK signaling pathway and a subsequent reduction in GRASP65 phosphorylation. The current study provided new information in the research of the cerebral ischemia-reperfusion injury mechanism. [ABSTRACT FROM AUTHOR]
- Published
- 2016
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