網膜缺血或實驗性青光眼---活血去瘀藥川芎內含成分之神經保護探討

趙效明
台北榮民總醫院
本研究所採用高眼壓網膜缺血模式（high intraocular pressure-induced retinal ischaemia），提供可重複性之網膜缺血，可檢測葯劑對「網膜缺血」或「實驗性青光眼」之療效。本模式雖和慢性青光眼有所不同，然而眼壓高於一定程度時將造成眼內血流減少及視神經盤之機械性壓迫（Hughes，1991），因而此模式至少可供探討青光眼的尚未瞭解之致病機轉（如它和膠質細胞衍生神經滋養因子或基質金屬蛋白酵素之關係）。「網膜缺血」或「實驗性青光眼」模式之建立﹔研究擬神經保護劑ferulic acid and tetramethylpyrazine﹙活血去瘀藥川芎萃取物﹚，對疾病模式的影響﹔藥物治療;，保護機轉為何？1. 釋放特定因子，保護變性的網膜細胞或延緩其死亡？2. 抵消毒性﹙鈣流、麩氨酸、游離基﹚？實施方法：實驗中將採用電器網膜生理圖、生化方法、鏈鎖反應、西方墨點法，以及組織病理學等方法。
關鍵字：網膜缺血；實驗性青光眼；基質金屬蛋白酵素;；川芎；神經滋養因子；麩氨酸；游離基。

Therapeutic Effects of Two Chinese Herbal Ingredients (Ferulic Acid and Tetramethylpyrazine) against Retinal Ischaemia or Experimental Glaucoma

shiau, ming-chao
Taipei Veteran General Hospital
An increase in intraocular pressure (IOP) to a certain level (e.g. beyond systolic blood pressure) can result in a reduction in ocular blood flow and mechanical compression in the optic nerve head region. An experimental glaucoma animal model is designed utilizing the anterior chamber cannulation to create a high intraocular pressure (HIOP) for 45 minutes. The HIOP procedure provides a reproducible and appropriate degree of retinal ischaemic changes (hypoxia/anoxia) and is considered as a satisfactory way to evaluate how defined agents affect retinal ischaemia/ reperfusion or experimental glaucoma. An investigation will be made into the underlying mechanism of glaucoma [e.g. its relationship with the expression of glia-derived neurotrophic factor (GDNF), and matrix metalloproteinase (MMP)].Whether the following agents would provide protective effects will also be evaluated. These include ferulic acid and tetramethylpyrazine, two active ingredients of a Chinese herbal medicine named Chuan Xiong (Liguusticum wallichi Franchat). Chuan Xiong is believed to act both as a vasodilator and as an anticoagulant ? What might be the mechanisms underlying the possible therapeutic effect of defined drugs?
關鍵字：retinal ischaemia；experimental glaucoma；extracellular matrix proteinases；ferulic acid；tetramethylpyrazine；neurotrophic factor；glutamate；hydroxyl radicals