摘要或動機

安非他命的濫用在台灣是非常嚴重的公眾健康及社會問題。安非他命會導致一連串的行\r
為異常，包括在中腦紋狀體內釋放多巴胺及阻止多巴胺回收來增加使用者的活動力。由於安\r
非他命會對腦細胞造成傷害，本研究的目的為探討低劑量、無立即毒性之安非他命(類似於人\r
類使用習慣)於短期內是否會對老鼠大腦紋狀體內的蛋白質表現有影響。因此利用西方點墨法\r
分析施打低劑量安非他命(2 到6 mg/kg)約一星期之後，C57BL6 小鼠的大腦紋狀體中一些重\r
要蛋白質[包括腺?酸受體A2A-R、第五亞型腺?酸環化?AC5、caspase-8、PARP、NF-κB\r
及血紅素加氧?-1(HO-1)]的表現是否有改變。實驗結果顯示，低劑量安非他命處理對大部分\r
蛋白質的表現並沒有明顯的差異，但在施打安非他命老鼠之大腦紋狀體中，HO-1 有些微但明\r
顯的增加，顯示安非他命可能對腦組織產生氧化性傷害。因此長期使用安非他命對中腦紋狀\r
體是否造成傷害是值得關心及繼續探討的課題。The wide spreading use of amphetamine (AMPH) in Taiwan has become a serious\r
public health and social problem. AMPH evokes a series of behavior abnormality including\r
enhanced locomotor behavior by releasing dopamine and inhibiting dopamine-uptake in the\r
striatum. Since AMPH is known to cause brain damage, the purpose of this study is to\r
investigate the expression of several important proteins in the mouse striatum after\r
treatment with low and non-toxic dosages of AMPH for a short period (mimicking the\r
common usage pattern of humans). C57BL6 mice were daily IP-injected with various doses\r
of AMPH (0 to 6 mg/kg) for one week. Expression levels of adenosine receptor A2A-R,\r
adenyl cyclase type 5,caspase-8, PARP, NF-κB and heme oxygenase-1 (HO-1) in the\r
striatum were analyzed by Western blotting technique. Most proteins examined were not\r
affected by the 1-week AMPH treatment, except HO-1. A slight but significant increase of\r
HO-1 by AMPH treatment indicated that AMPH may cause oxidative damage in brain.\r
These results suggest that the injury induced by long-term AMPH exposure warrants our\r
further concerns and investigation.