頁籤選單縮合
題名 | Effects of Tamoxifen on Traumatic Brain Injury-induced Depression in Male Rats |
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作者姓名(外文) | Wang, Che-chuan; Wee, Hsiao-yue; Chio, Chung-ching; Hu, Chiao-ya; Kuo, Jinn-rung; | 書刊名 | Formosan Journal of Surgery |
卷期 | 49:3 2016.06[民105.06] |
頁次 | 頁101-109 |
分類號 | 418.214 |
關鍵詞 | Depression-like behavior; Extracellular signal-regulated kinases; Forced swim test; Selective estrogen receptor modulator; Tamoxifen; |
語文 | 英文(English) |
英文摘要 | Background/Introduction: Previous studies have investigated the neuroprotective effects of tamoxifen (TMX), but its antidepressant-like effects in traumatic brain injury (TBI) remain unclear. Purposes/Aims: The present study was conducted to determine whether TMX can attenuate TBI-induced depression-like behavior and whether this effect involves the activation of extracellular signal-regulated kinase 1/2 (ERK1/2). Methods: Anesthetized male SpragueeDawley rats were divided into four groups: shamoperated controls, TBI controls, TBI þ TMX treatment (1 mg/kg), and TMX (1 mg/ kg) þ ERK1/2 antagonist, SL327 (30 mg/kg). Depression-like behaviors were evaluated through forced swim tests on Day 4, Day 8, and Day 15. On Day 15 after TBI, phosphorylated ERK1/2 (pERK1/2) expression was investigated by Western blotting; neuronal apoptosis, p-ERK1/2, B-cell chronic lymphocytic leukemia/lymphoma 2 (BCL2), and brain-derived neurotrophic factor (BDNF ) expression in neuronal cells were evaluated using double immunofluorescence. Results: On Day 15 after TBI, TMX significantly reduced the duration of TBI-induced immobility compared with the TBI controls. The frequency of neuronal apoptosis and numbers of BCL2- positive, BDNF-positive, and p-ERK1/2-positive neuronal cells in hippocampal CA3 were significantly improved by TMX. However, these TMX effects were significantly blocked by SL327 administration. Conclusion: Our results suggest that intraperitoneal injection of TMX may ameliorate TBIinduced depression-like behavior in rats by increasing neuronal p-ERK1/2 expression, which may be associated with neuronal Bcl2 and BDNF expression and decreased neuronal apoptosis. |
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