Satoh Itaru, Saito Motoaki, Kinoshita Yukako, Shomori Kohei, Suzuki Hiroto, Yamada Masashi, Kono Tomoharu, Satoh Keisuke
Department of Pathophysiological and Therapeutic Science, Division of Molecular Pharmacology, Tottori University Faculty of Medicine, 86 Nishimachi, Yonago 683-8503, Japan.
Life Sci. 2005 Sep 2;77(16):2030-9. doi: 10.1016/j.lfs.2005.04.022.
In order to investigate the diabetes-associated neuropathy and prevent effects of cyclohexenonic long-chain fatty alcohol, a neurotrophic substance, in trachea, we studied its effect on streptozotocin-diabetic hyper-reactivity in the rat trachea. Diabetes was induced in 8-week-old male Sprague-Dawley rats by administering an intraperitoneal injection of streptozotocin (50 mg/kg). The rats were divided randomly into four groups and were maintained for four weeks: age-matched control rats, diabetic rats without treatment with cyclohexenonic long-chain fatty alcohol, and diabetic rats treated with cyclohexenonic long-chain fatty alcohol (2 and 8 mg/kg, i.p. every day). The serum glucose and insulin levels were determined, and the contractile responses of the trachea induced by carbachol and KCl were investigated. Treatment with cyclohexenonic long-chain fatty alcohol did not alter the rats' diabetic status, i.e., body weight, thickness of the trachea, serum glucose levels, and serum insulin levels, but significantly improved the diabetic-induced hyper-reactivity of the rat trachea in a dose-dependent manner. There was no significant difference in either the carbachol- or KCl-induced contractile forces between groups with or without mucosa in the functional studies. In histological examinations, thinning of cricoid cartilage, thickness of basal membrane, and degeneration, fragmentation of elastic fibers in the submucosal layer, and hypertrophy of smooth muscle bundle in the membranous wall of trachea were observed in the diabetic rat trachea, which were improved by treatment with cyclohexenonic long-chain fatty alcohol. Our data indicate that this drug can prevent hyper-reactivity in the diabetic trachea.
为了研究糖尿病相关神经病变以及气管中神经营养物质环己烯基长链脂肪醇的预防作用，我们研究了其对链脲佐菌素诱导的糖尿病大鼠气管高反应性的影响。通过腹腔注射链脲佐菌素（50mg/kg）诱导8周龄雄性Sprague-Dawley大鼠患糖尿病。将大鼠随机分为四组并维持四周：年龄匹配的对照大鼠、未用环己烯基长链脂肪醇治疗的糖尿病大鼠以及用环己烯基长链脂肪醇治疗的糖尿病大鼠（2mg/kg和8mg/kg，每天腹腔注射）。测定血清葡萄糖和胰岛素水平，并研究卡巴胆碱和氯化钾诱导的气管收缩反应。用环己烯基长链脂肪醇治疗并未改变大鼠的糖尿病状态，即体重、气管厚度、血清葡萄糖水平和血清胰岛素水平，但以剂量依赖方式显著改善了糖尿病诱导的大鼠气管高反应性。在功能研究中，有或没有黏膜的组之间，卡巴胆碱或氯化钾诱导的收缩力没有显著差异。在组织学检查中，在糖尿病大鼠气管中观察到环状软骨变薄、基底膜厚度、黏膜下层弹性纤维变性、断裂以及气管膜壁平滑肌束肥大，用环己烯基长链脂肪醇治疗可改善这些情况。我们的数据表明，这种药物可以预防糖尿病气管的高反应性。
