Solmaz Volkan, Çınar Bilge Piri, Yiğittürk Gürkan, Özlece Hatice Köse, Avni Eroglu Hüseyin, Tekatas Aslan, Erbaş Oytun, Taşkıran Dilek
Trakya University Faculty of Medicine, Department of Neurology, Edirne, Turkey.
Samsun Training and Reseach Hospital, Department of Neurology, Samsun, Turkey.
Biomed Pharmacother. 2017 May;89:468-472. doi: 10.1016/j.biopha.2017.02.027. Epub 2017 Feb 27.
The purpose of the present study is to investigate the possible healing effects of octreotide (OCT) on motor performance, electrophysiological and histopathological findings of diabetic neuropathy in a rat model of diabetes mellitus (DM). To induce diabetes, rats were administered a single dose (60mg/kg) of streptozotocin (STZ). Diabetic rats were treated either with saline (1ml/kg/day, n=7) or OCT (0.1mg/kg/day, n=7) for four weeks. Seven rats served as control group and received no treatment. At the end of the study, electromyography (EMG), gross motor function (inclined plate test), general histology and the perineural thickness of sciatic nerve were evaluated. At the end of study, weight loss was significantly lower in OCT treated rats than that of saline treated ones (p<0.001). Electrophysiologically, compound muscle action potential (CMAP) amplitudes of the saline treated DM group were significantly reduced than those of controls (p<0.0001). Also, distal latency and CMAP durations were significantly prolonged in saline treated DM group (p<0.05) compared to control. However, treatment of diabetic rats with OCT significantly counteracted these alterations in EMG. Furthermore, OCT significantly improved the motor performance scores in diabetic rats (p<0.05). Histomorphometric assessment of the sciatic nerve demonstrated a significant reduction in perineural thickness in OCT treated group compared to saline group. In conclusion, OCT possesses beneficial effects against STZ-induced diabetic neuropathy, which promisingly support the use of OCT as a neuroprotective agent in patients with diabetic neuropathy.
本研究的目的是在糖尿病(DM)大鼠模型中,研究奥曲肽(OCT)对糖尿病性神经病变的运动功能、电生理和组织病理学结果的可能治疗作用。为诱导糖尿病,给大鼠单次注射链脲佐菌素(STZ,60mg/kg)。糖尿病大鼠用生理盐水(1ml/kg/天,n = 7)或奥曲肽(0.1mg/kg/天,n = 7)治疗四周。七只大鼠作为对照组,未接受治疗。在研究结束时,评估肌电图(EMG)、总体运动功能(斜板试验)、一般组织学和坐骨神经的神经周厚度。研究结束时,奥曲肽治疗的大鼠体重减轻明显低于生理盐水治疗的大鼠(p<0.001)。在电生理方面,生理盐水治疗的糖尿病组复合肌肉动作电位(CMAP)幅度比对照组明显降低(p<0.0001)。此外,与对照组相比,生理盐水治疗的糖尿病组远端潜伏期和CMAP持续时间明显延长(p<0.05)。然而,用奥曲肽治疗糖尿病大鼠显著抵消了这些EMG改变。此外,奥曲肽显著改善了糖尿病大鼠的运动功能评分(p<0.05)。坐骨神经的组织形态计量学评估显示,与生理盐水组相比,奥曲肽治疗组的神经周厚度显著降低。总之,奥曲肽对STZ诱导的糖尿病性神经病变具有有益作用,有望支持将奥曲肽用作糖尿病性神经病变患者的神经保护剂。