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研究生:李孟璁
研究生(外文):Meng-Tsung Lee
論文名稱:甲基安非他命誘發小鼠紋狀體表現第一型血基質氧化酶之機制探討
論文名稱(外文):The Mechanism of Methamphetamine-induced Heme Oxygenase-1 Expression in Mouse Striatum
指導教授:嚴錦城
指導教授(外文):Jiin-Cherng Yen
學位類別:碩士
校院名稱:國立陽明大學
系所名稱:藥理學研究所
學門:醫藥衛生學門
學類:藥學學類
論文種類:學術論文
論文出版年:2009
畢業學年度:97
語文別:中文
論文頁數:65
中文關鍵詞:甲基安非他命第一型血基質氧化酶
外文關鍵詞:MethamphetamineHeme Oxygenase-1
相關次數:
  • 被引用被引用:0
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  • 下載下載:16
  • 收藏至我的研究室書目清單書目收藏:0
甲基安非他命具有強烈的中樞興奮作用,具有成癮性,產生生理及心
理方面許多嚴重的問題。甲基安非他命作用於單胺類神經末梢,主要機轉
是讓單胺類物質大量釋放至突觸間隙,並阻止其回收。在多巴胺神經末
梢,甲基安非他命會減少多巴胺轉運子 (dopamine transporter) 的數量。
氧化性壓力增加於甲基安非他命的神經毒性中扮演重要的角色,氧化性壓
力的來源包括superoxide、peroxynitrite、多巴胺自我氧化等,利用提升細
胞抗氧化能力的方法可能減少甲基安非他命所造成的傷害。
第一型血基質氧化酶 (heme oxygenase-1, HO-1),是一種可以被誘發
的蛋白質,同時也是屬於熱休克蛋白 (heat shock protein) 的一員。HO-1
催化的代謝產物及本身都具有抗氧化的功能,扮演細胞保護的角色。我們
實驗室之前的研究發現甲基安非他命會誘發小鼠紋狀體HO-1 產生,且扮
演降低神經毒性的角色。其後利用細胞實驗模式,證明甲基安非他命透過
活化PI3K/Akt/Nrf2 路徑而使HO-1 表現量增加。但於動物模式實驗中,
甲基安非他命誘發HO-1 表現的機轉仍不清楚。因此本研究擬探討HO-1
在動物模式中減輕甲基安非他命所致神經傷害的分子機制。
本研究發現前處理HO-1 活性抑制劑ZnPP 後,會增加甲基安非他命
的神經毒性,顯示HO-1 可能具有神經保護功能。進一步前處理兩種自由
基清除劑(c-PTIO、DMTU)後發現會使甲基安非他命誘發小鼠紋狀體的
HO-1 表現量減少。因此,甲基安非他命誘發小鼠紋狀體表現HO-1 可能
與ROS 的產生有關係。本研究亦發現,腹腔投與甲基安非他命(20 mg/kg)
誘發小鼠紋狀體HO-1 的表現量於12~24 小時增加至最高峰,磷酸化Akt
的表現量在6~12 小時增加至最高峰,此一現象符合時間的先後順序的相關性。前處理PI3K 抑制劑LY294002 或wortmannin 後,會使甲基安非他
命誘發小鼠紋狀體磷酸化Akt 及HO-1 的表現量減少。進一步利用紋狀體
內注射PI3K 抑制劑的方式,不但得到類似的實驗結果,亦同時確認了甲
基安非他命是透過活化紋狀體中PI3K 而誘發HO-1 的表現。因此實驗結
果顯示,甲基安非他命可能經由PI3K/Akt 路徑誘發小鼠紋狀體中HO-1
的表現。文獻指出,多巴胺作用在D2 receptor 會導致Akt 去磷酸化,因此
本研究利用前處理兩種D2 receptor 的拮抗劑(haloperidol、remoxipride)去排
除此一效應。
綜合本研究之結果,可知動物實驗模式中,甲基安非他命於小鼠紋狀
體誘發之HO-1 具有神經保護功能。甲基安非他命可能經由PI3K/Akt 路
徑誘發小鼠紋狀體HO-1 的表現
Methamphetamine (METH) is a powerful and widely abused
psychostimulant. METH causes damage to dopaminergic nerve terminals of
animals. In addition, decreases in dopamine transporter (DAT) by METH may
be mediated by reactive oxidative species (ROS) and oxidative stress.
Oxidative stress has been shown to play an important role in METH-induced
neurotoxicity. Enhancement of antioxidant mechanisms could reduce
METH-induced neurotoxicity.
Heme oxygenase-1 (HO-1) is a 32 kDa member of the heat shock protein
superfamily that catalyzes the oxidative degradation of heme to biliverdin in
brain and other tissues. HO-1 may protect cells by promoting the catabolism
of heme to several byproducts (biliverdin, bilirubin) with free radical
scavenging capabilities. Previous studies of our laboratory have shown that
the antioxidative enzyme HO-1 is induced by METH treatment and exhibits
neuroprotective effect against METH-induced neurotoxicity in mice. Recently,
our laboratory further demonstrated that METH-induced HO-1 expression was
dependent on activation of PI3K/Akt pathway in SH-SY5Y neuroblastoma
cells. However, the molecular mechanism of HO-1 expression induced by
METH is still unclear in animal model.
This study was aimed to clarify the protective role of HO-1 against
METH-induced neurotoxicity and the involvement of PI3K/Akt pathway in
METH-induced HO-1 increases in mouse striatum. First, this study
demonstrated that intraperitoneal injection of METH (20 mg/kg) increased theprotein level of HO-1 in mouse striatum in a time-dependent manner with a
peak increase at 12-24 hours after METH administration. In addition, this
study also analyzed HO-1 mRNA expression by real-time PCR, and found that
HO-1 mRNA was increased at 12-24 hours after METH treatment. To further
confirm METH-induced HO-1 expression was related to ROS, two different
free radical scavengers (c-PTIO and DMTU) were used to block ROS
generation. It was found that METH-induced HO-1 expression was reduced at
24 hours. Furthermore, this study also evaluated whether HO-1 plays a
neuroprotective role against METH-induced neurotoxicity by pretreatment
with ZnPP (HO-1 activity inhibitor). The data showed that ZnPP could
enhance METH-induced neurotoxicity markedly. Therefore, METH-induced
HO-1 may have a neuroprotective function.
Moreover, the protein level of phospho-Akt was also increased at 6-12
hours after METH treatment. This study further found that PI3K inhibitors
(LY294002 or wortmannin) significantly reduced striatal HO-1 expression.
METH-induced HO-1 expression in mouse striatum was also found to be
attenuated by bilateral intra-striatal microinjections of LY294002. However, it
is reported that activation of D2 dopamine receptor could inhibit Akt
phosphorylation. Therefore, D2 dopamine receptor antagonists (haloperidol
and remoxipride) were used to rule out the confounding effect of D2-mediated
deactivation of Akt signaling. The results showed that the levels of
phospho-Akt were elevated by D2 dopamine receptor antagonists.
These results suggested that HO-1 might be induced by METH and could
play a neuroprotective role against METH-induced neurotoxicity through the
PI3K/Akt signaling pathway in mouse striatum.
誌謝.................................................................................................................... i
目次.................................................................................................................... i
圖次..................................................................................................................iii
摘要................................................................................................................... 1
Abstract .............................................................................................................. 1
研究背景........................................................................................................... 3
甲基安非他命 (methamphetamine, METH) ..................................... 3
甲基安非他命與氧化性壓力............................................................. 4
第一型血基質氧化酶 (heme oxygenase-1, HO-1)........................... 6
Phosphatidylinositol 3-kinase (PI3K) pathway 與HO-1 ................... 7
甲基安非他命與HO-1 ...................................................................... 8
研究目的........................................................................................................... 9
材料及方法..................................................................................................... 10
一、實驗動物................................................................................... 10
二、藥物投與................................................................................... 10
三、紋狀體取樣............................................................................... 11
四、組織蛋白質萃取....................................................................... 11
五、組織蛋白質定量....................................................................... 12
六、西方墨點法(Western blotting) ............................................ 12
七、即時定量聚合酶連鎖反應法 (real-time PCR)....................... 13
八、實驗藥品及材料來源............................................................... 14
九、統計方法................................................................................... 16
實驗設計......................................................................................................... 17
一、確立甲基安非他命引起小鼠紋狀體神經毒性之劑量.......... 17
二、確立甲基安非他命誘發小鼠紋狀體表現HO-1 之時間....... 17
三、探討甲基安非他命誘發小鼠紋狀體表現HO-1 是否具有神經
保護功能................................................................................... 17
四、探討甲基安非他命是否可藉由ROS 的產生而誘發小鼠紋狀
體表現HO-1 ............................................................................ 18
五、探討甲基安非他命是否經由PI3K/Akt 路徑使小鼠紋狀體核區
表現HO-1 ................................................................................ 18
研究結果......................................................................................................... 19
一、甲基安非他命引起小鼠紋狀體神經毒性之劑量.................. 19
ii
二、甲基安非他命誘發小鼠紋狀體表現HO-1 之時間關係....... 19
三、甲基安非他命所誘發HO-1 具有神經保護功能................... 20
四、甲基安非他命可藉由ROS 的產生而誘發小鼠紋狀體表現
HO-1.......................................................................................... 21
五、甲基安非他命經由PI3K/Akt 路徑使小鼠紋狀體表現HO-122
六、D2 receptor 對甲基安非他命誘發小鼠紋狀體p-Akt 及HO-1
之影響....................................................................................... 24
討論................................................................................................................. 26
一、甲基安非他命引起小鼠紋狀體神經毒性之適合劑量.......... 26
二、甲基安非他命誘發小鼠紋狀體表現HO-1 之時間關係....... 26
三、甲基安非他命誘發小鼠紋狀體表現HO-1 之功能............... 28
四、ROS 與甲基安非他命誘發小鼠紋狀體表現HO-1 之關係.. 29
五、PI3K/Akt 路徑與甲基安非他命誘發小鼠紋狀體表現HO-1 之
關係........................................................................................... 29
六、麻醉劑對甲基安非他命誘發小鼠紋狀體Akt 磷酸化及HO-1
表現之影響............................................................................... 31
七、D2 receptor 對甲基安非他命誘發小鼠紋狀體p-Akt 及HO-1
之影響....................................................................................... 31
結論................................................................................................................. 34
參考文獻......................................................................................................... 35
圖表................................................................................................................. 44
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