| 摘要: | 糖尿病為一種複雜的代謝疾病，包括第一型糖尿病(胰島素依賴型)是由於自體免疫系統破壞產生胰島素的β細胞所導致與第二型(或懷孕妊娠)糖尿病(非胰島素 依賴型)是由於體內產生胰島素抵抗。若控制高血糖、降糖藥物（第2型糖尿病）和胰島素補充尚無法控制病情，將會引起一些急性併發症，例如高血糖症或酮症酸 中毒。長期併發症包括視網膜病變、慢性腎衰竭及神經病變。糖尿病周邊神經病變是糖尿病最常引起神經病變性疼痛的其中一種原因。經皮神經電刺激已知有效治療 糖尿病周邊神經病變，超音波能治療腕隧道症候群所造成的疼痛與皮膚感覺異常。我們的研究結果發現敵芬尼朵是一強效的鈉離子通道阻斷劑，而電位依賴性鈉離子 通道在神經病變性疼痛中扮演一重要的角色。甚者，雖然目前對於糖尿病神經病變性疼痛之機轉尚未完全清楚，一般可接受的理論與氧化壓力和細胞凋亡有關。因此 我們的計畫中將探討敵芬尼朵、經皮神經電刺激、超音波或合併敵芬尼朵與經皮神經電刺激(或超音波)治療第一、二型糖尿病之周邊神經病變在神經行為、組織 學、細胞激素、膠細胞活性、氧化壓力與神經凋亡之情形作整合性探討。計畫預設為四年計畫，第一年：探討痛覺過敏、觸覺過敏與神經組織學；第二年：探討細胞 激素與膠細胞活性；第三年：探討氧化壓力；最後一年：探討細胞凋亡。
Diabetes mellitus is a metabolic disorder resulting from a defect in insulin secretion, insulin action, or both. Diabetes mellitus develops due to a diminished production of insulin (type 1) or resistance to its effects (type 2 and gestational). If the disease is not adequately controlled by glycemic control, drug (type 2) and insulin use, acute complications (hypoglycemia or ketoacidosis) may occur. Serious long-term complications include retinal damage, chronic renal failure, and nerve damage (neuropathy). Diabetic peripheral neuropathy is one of the most common causes of neuropathic pain. Transcutaneous electrical nerve stimulation (TENS) therapy is known to be an effective and safe strategy in treatment of symptomatic diabetic peripheral neuropathy. Ultrasound can treat for pain and paresthesias in the distribution of the median nerve of carpal tunnel syndrome. Our recent study showed that diphenidol is a potent sodium channel blocker. In addition, voltage-dependent sodium channels play an important role in neuropathic pain. Furthermore, the cellular and molecular background underlying neuropathic pain behavior is not clear, but it is widely accepted that both oxidative stress and apoptosis mechanisms could be involved. Therefore, our project will emphasize the effects of diphenidol, TENS, ultrasound or combined diphenidol and TENS (ultrasound) on the peripheral neuropathy of type 1 and type 2 diabetic rats, comparing the temporal profiles of neuro-behavior, histology, cytokines, glial activity, oxidative stress, and apoptosis. This project will be carried out for four years. First year: the evaluation of hyperagelsia, allodynia, and histology; second year: the evaluation of cytokine and glial activity; third year: the evaluation of oxidative stress; last year: the evaluation of apoptosis. |
