個人簡要經歷

亞洲大學 生活應用科學系 助理教授2001/08-
亞洲大學動物實驗管理小組審查委員兼執行秘書 2002-
第五屆及第六屆工程科技與中西醫學應用研討會議程委員 2002，2003
台中榮民總醫院 教學研究部 博士後研究 2000/07至2001/08

期刊論文

1. Min-Min Lee, Ming-Tsueh Hseih, Jon-Son Kuo, Feng-Tsgh Yeh and, Hsueh-Meei Huang. Magnolol protects cortical neuronal cells from chemical hypoxia in rats. Neuroreport 9 :3451-3456, 1998. （SCI）
2. Min-Min Lee, Hsueh-Meei Huang, Ming-Tsueh Hseih, Chung-Shing Chen, Feng-Tsgh Yeh and Jon-Son Kuo. Anti-inflammatory and neuroprotective effects of magnolol in chemical hypoxia in rat cultured cortical cells in hypoglycemic media. Chinese Journal of Physiology 43 (2):1-8, 2000

參加研討會發表論文一覽表

編號 系別 姓名 研討會日期 研討會名稱 論文題目 備註
生應系 李明明 2003 第六屆工程科技與中西醫學應用研討會 有效中藥網路自動化搜尋資料庫
生應系 李明明 2003 第六屆工程科技與中西醫學應用研討會 電刺激合谷與內關穴對經絡能量值變化之探討
生應系 李明明 2002 第十七屆天然藥物研討會計中草藥生物科技研討會 川芎活性成分對麩胺酸引起鼠腦細胞傷害的保護作用
生應系 李明明 2002 第五屆工程科技與中西醫學應用研討會 川芎活性成分的細胞保護作用-對活性氧原子自由基生成作用的影響
生應系 李明明 2002 The 3rd Symposium of cerebral citculation and metabolism Effect of naloxone on cell injury induced by extracellular hydroxyl radicals by spectrofluorometric detection in primary rat mixed cortical cultures
生應系 李明明 2001 Brain'01國際腦血流及代謝研討會 Effect of naloxone on free radical generation induced by hypoxia/reoxygenation in rat cortical mixed cultured cells
生應系 李明明 2001 Brain'01國際腦血流及代謝研討會 Effect of magnolol on glutamate metabolic processes induced by KCN in rat cortical mixed cultured cells.
生應系 李明明 2000 中華民國神經醫學聯合學術研討會 厚朴酚對化學性缺氧之鼠腦皮質細胞的抗炎及神經保護性作用

曾經參與研究計劃表

編號 姓名 Source of support Title of support Name/role on project Duration of support Funding(in 1000 NT$)
1 李明明 台中榮總院內計畫TCVGH-907301C 厚朴酚對培養大鼠腦皮質神經細胞-神經膠細胞缺氧/缺糖後細胞麩胺酸及乳酸代謝過程的影響 共同研究人員 90.1-90.12 1000
2 李明明 台中榮總院內計畫TCVGH-907309D 納洛酮在老鼠腦缺血之神經保護作用 博士後研究員 90.1-90.12 1000
3 李明明 台中榮總院內計畫TCVGH-907323A 納洛酮對培養大鼠腦皮質細胞受到氫氧自由基刺激後細胞損傷的影響 共同研究人員 90.1-90.12 250
4 李明明 台中榮總院內計畫TCVGH-917323D 川芎活性成份川芎口秦 對培養初生大鼠腦皮質神經細胞-神經膠細胞因麩胺酸引起細胞損傷的保護機制 計劃主持人 91.1-91.12 790
5 李明明 台中榮總院內計畫TCVGH-917310D 川芎活性成份川芎秦對大鼠腦缺血/再灌流後引起細胞內生性抗氧化酵素活性變化的影響 協同主持人 91.1-91.12 800
6 李明明 國科會專題計劃NSC 91-2320-B-468-002 川芎活性成分對缺氧之鼠腦細胞內生性抗氧化酵素的影響 計劃主持人 91.8-92.7 550
7 李明明 國科會專題計劃(申請中) 川芎活性成分對大鼠局部性腦缺血/再灌流引起神經細胞傷害的保護作用-細胞凋亡的影響 計劃主持人 92.8-93.7

(1)腦中風，造成老年人口的主要死亡原因，因此研究一有效藥物以對抗中風後造成的嚴重損傷進而治癒其造成之後遺症，一直是從事研究工作者努力的目標。氰化鉀中毒已被普遍使用作為化學性缺氧的實驗模式，其造成細胞代謝性障礙，影響細胞對能量來源的利用，造成能量來源空乏。本研究室初步結果顯示厚朴酚可以有效減輕缺氧性傷害所致的神經元細胞數目減少並維持細胞形態的完整性，降低乳酸脫氫脢的釋放，抑制缺氧炎性反應產生的前列腺素及一氧化氮。本研究目的進一步評估缺氧狀況下的神經傷害，並評估厚朴酚的治療效果，是否經由調節細胞代謝過程來保護細胞免於缺氧性傷害。實驗中利用培養初生鼠大腦皮質細胞，分析缺氧狀況下細胞外乳酸脫氫脢釋放量及乳酸堆積量以評估細胞損傷程度；利用酵素分析法分析細胞外蓄積之麩胺酸，以評估細胞遭受之興奮性毒性；利用免疫墨點法及免疫染色法分析麩胺酸代謝酵素---麩胺酸脫氫脢 (GDH)及麩氨合成脢 (GS)；以及乳酸代謝酵素 (LDH)。而維持正常的代謝功能有賴細胞膜的完整性，所以將利用免疫墨點法分析細胞膜上麩胺酸及乳酸傳送體的表現。本研究結果可進一步提供厚朴酚對抗缺氧性傷害的確實作用機制，俾供將來臨床應用之參考。

Stroke, a major cause of death and disability to the elderly, often results in delayed neurological morbility or mortality. Potassium cyanide (KCN) intoxication has often been used as a model of chemical hypoxia. It may cause cellular metabolic disorders, affect cell utilization of energy source and result in energy depletion. Our preliminary results demonstrated that magnolol, an active compound of magnolia officinalis, may attenuate the KCN-induced neuronal injury and morphological impairment, decrease the extracellular lactate dehydrogenase (LDH) release, attenuate the production of prostaglandin and nitric oxide induced by hypoxic-inflammatory response. The overall aims of this study are further to evaluate whether magnolol may modulate cellular metabolic processes to protect cell against hypoxic injuries in rat cortical neuron-glia mixed cultured cells. Hypoxic injury will be produced by exposure of the culture cells to KCN in the glucose-free medium. Severity of cell injury will be evaluated on release of lactate dehydrogenase (LDH). Extracellular glutamate levels will be assessed by an enzymatic method. Protein levels and activities of intracellular glutamate metabolic enzymes (GDH and GS), and lactate metabolic enzyme activity (LDH) will be evaluated by immunoblotting and immunostaining method. Normal metabolic function of cells is dependent on integrity of cell membrane, and these will be assessed by examining transporters for glutamate and lactate. This study may further clarify whether the mechanism of neuronal protective effect of magnolol against hypoxia/hypoglycemia injury involves improvement of energy metabolism and integrity of cell membrane.

(2)腦中風，造成老年人口的主要死亡原因。本研究的主要目的在探討大鼠腦皮質培養細胞在缺氧/低糖/回氧 (hypoxia/hypoglycemia/reoxygenation, 以下簡稱HO/HG/RO) 後引起的神經傷害，並探討鴉片類接受體拮抗劑-納洛酮 (naloxone)保護神經受傷害是否涉及保護細胞膜上神經傳遞物(neurotransmitters)及能量受質(energy substance)之載體(transporters)。
本研究將利用缺氧箱 (hypoxic chamber) 灌流95% N2, 5% CO2以產生HO/HG/RO 的傷害。將分析乳酸脫氫酵素 (lactate dehydrogenase; LDH) 的釋放量，以評估對細胞的傷害。將利用酵素分析法及高效液相層析法 (HPLC) 定量出細胞內外神經傳遞物及能量受質之含量，包括細胞內外兒茶酚胺，麩胺酸，葡萄糖及乳酸含量，藉由蛋白質的定量分析及免疫化學染色方法定出細胞膜上神經傳遞物及能量受質之載體蛋白質活性，分析項目包括葡萄糖載體（glucose transporter: GLUT-1, GLUT-3），麩胺酸載體（glutamate transporter: GLT-1, EAAC1, GLAST），乳酸載體（lactate transporter : MCT1 and MCT2）和兒茶酚胺載體 (catecholamine transporters)。本研究將檢測檢測納洛酮是否可以有效保護這些載體，減輕傷害。
預期納洛酮可以保護這些載體的活性。研究結果可能有助於臨床上預防或治療腦缺血或中風之參考。

Stroke, a major cause of death and disability to the elderly often results in delayed neurological morbility or mortality. The overall aims of these studies are to evaluate the mechanism of hypoxia/hypoglycemia/reoxygenation (HO/HG/RO)- induced neuronal cell injury in rat cortical cultured cells and to investigate whether protection against the cell injury by naloxone, an opiate receptor antagonist, involves protection on the cellular membrane transporters of neurotransmitters and energy substances.
The present study will examine the neuronal cytotoxicity induced by HO/HG/RO with infusing anoxic gas (95% N2 and 5% CO2) in a hypoxic chamber. The cell injury will be assessed by lactate dehydrogenase (LDH) release in the media. The neurotransmitters and energy substrates concentration in extracellular or intracellular spaces will be assessed by enzymatic method and HPLC assay, including catecholamines, glutamate, glucose and lactate. The transporters protein expressions and activities will be assessed by immunoblotting and immunocytochemical methods, including GLUT-3 and GLUT-1 (glucose transporters), EAAC1, GLT-1 and GLAST (glutamate transporters), MCT1 and MCT2 (lactate transporter) and catecholamine transporters (ET, NET, SERT, DAT). We further test whether naloxone prevent these transporters from HO/HG/RO injury.
We expect that naloxone may protect the activities of above mentioned transporters. The obtained results will give some light on the understanding of protective mechanism of naloxone. An implication of this drug in prevention and therapy of stroke is also suggested.