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丁香酚对链脲佐菌素诱导的糖尿病大鼠神经和血管功能障碍的影响。

Effects of eugenol on nerve and vascular dysfunction in streptozotocin-diabetic rats.

作者信息

Nangle Matthew R, Gibson T Michael, Cotter Mary A, Cameron Norman E

机构信息

School of Medical Sciences, University of Aberdeen, Aberdeen, Scotland, UK.

出版信息

Planta Med. 2006 May;72(6):494-500. doi: 10.1055/s-2005-916262.

Abstract

Hyperglycaemia in diabetes mellitus results in oxidative stress and pro-inflammatory changes which contribute to vascular complications including endothelial dysfunction and peripheral neuropathy. The aim of this study was to examine whether treatment with the dominant ingredient of clove oil, eugenol, which has antioxidant and anti-inflammatory properties, could improve diabetic vascular and nerve function in streptozotocin-induced diabetic rats. Intervention treatment was given for 2 weeks following 6 weeks of untreated diabetes. Dose-ranging studies on diabetic deficits in sciatic nerve motor and saphenous nerve sensory nerve conduction velocities gave ED50 values of 28 mg/kg and 9 mg/kg, respectively, conduction velocity being within the non-diabetic range at a dose of 200 mg/kg. Sciatic nerve endoneurial blood flow was 49% reduced by diabetes and this was completely corrected by 200 mg/kg eugenol treatment. Gastric fundus maximum nitrergic nerve-mediated relaxation was 44% reduced by diabetes; eugenol corrected this deficit by 69%. For renal artery rings, maximum endothelium-dependent relaxation to acetylcholine was 51% reduced by diabetes; eugenol corrected this deficit by 60%, with improvements in both nitric oxide and endothelium-derived hyperpolarising factor (EDHF)-mediated vasorelaxation components. Diabetes increased renal artery sensitivity to phenylephrine-mediated contraction, however, this was unaffected by eugenol treatment. Thus, aspects of both vascular and neural complications in experimental diabetes are improved by eugenol, which could have potential therapeutic implications for diabetic neuropathy and vasculopathy.

摘要

糖尿病中的高血糖会导致氧化应激和促炎变化,进而引发包括内皮功能障碍和周围神经病变在内的血管并发症。本研究的目的是检验具有抗氧化和抗炎特性的丁香油主要成分丁香酚治疗是否能改善链脲佐菌素诱导的糖尿病大鼠的糖尿病血管和神经功能。在未经治疗的糖尿病持续6周后进行了2周的干预治疗。对坐骨神经运动和隐神经感觉神经传导速度的糖尿病缺陷进行的剂量范围研究得出,ED50值分别为28 mg/kg和9 mg/kg,在200 mg/kg的剂量下传导速度处于非糖尿病范围内。糖尿病使坐骨神经内膜血流量减少了49%,而200 mg/kg丁香酚治疗可使其完全恢复正常。糖尿病使胃底最大一氧化氮能神经介导的舒张功能降低了44%;丁香酚使这一缺陷纠正了69%。对于肾动脉环,糖尿病使对乙酰胆碱的最大内皮依赖性舒张功能降低了51%;丁香酚使这一缺陷纠正了60%,一氧化氮和内皮衍生超极化因子(EDHF)介导的血管舒张成分均有所改善。糖尿病增加了肾动脉对去氧肾上腺素介导的收缩的敏感性,然而,丁香酚治疗对此无影响。因此,丁香酚可改善实验性糖尿病中血管和神经并发症的多个方面,这可能对糖尿病神经病变和血管病变具有潜在的治疗意义。

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