Oghbaei Hajar, Mohaddes Gisou, Hamidian GholamReza, Keyhanmanesh Rana
Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran.
Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
J Diabetes Metab Disord. 2020 Jan 13;19(1):105-113. doi: 10.1007/s40200-019-00481-4. eCollection 2020 Jun.
The purpose of the study was to evaluate the possible protective effects of low dose sodium nitrate preconditioning on the peripheral neuropathy in streptozotocin (STZ)-induced diabetic model.
Male Wistar rats were randomly divided into five groups: control (no intervention), control treated sodium nitrate (100 mg/L in drinking water), diabetic (no intervention), diabetic treated NPH insulin (2-4 U), and diabetic treated sodium nitrate (100 mg/L in drinking water). Diabetes was induced by intraperitoneal injection of STZ (60 mg/kg). All interventions were done for 60 days immediately following diabetes confirmation. Thermal and mechanical algesia thresholds were measured by means of hot-plate test, von Frey test, and tail-withdrawal test before the diabetic induction and after diabetes confirmation. At the end of the experiment, serum NOx level and serum insulin level were assessed. Blood glucose concentration and body weight have recorded at the base and duration of the experiment.
Both hypoalgesia, hyperalgesia along with allodynia developed in diabetic rats. Significant alterations including, decrease in tail withdrawal latency (30th day), decreased mechanical threshold (60th day), and an increase in hot plate latency (61st day) were displayed in diabetic rats compared to control rats. Nitrate and insulin preconditioning produced protective effects against diabetes-induced peripheral neuropathy. Data analysis also showed a significant increase in glucose level as well as a considerable reduction in serum insulin and body weight of diabetic rats, which restored by both insulin and nitrate preconditioning.
Sodium nitrate preconditioning produces a protective effect in diabetic neuropathy, which may be mediated by its antihyperglycemic effects and increased serum insulin level.
本研究旨在评估低剂量硝酸钠预处理对链脲佐菌素（STZ）诱导的糖尿病模型周围神经病变的潜在保护作用。
雄性Wistar大鼠随机分为五组：对照组（无干预）、接受硝酸钠处理的对照组（饮用水中含100 mg/L硝酸钠）、糖尿病组（无干预）、接受中性鱼精蛋白锌胰岛素（NPH胰岛素）治疗的糖尿病组（2 - 4 U）以及接受硝酸钠治疗的糖尿病组（饮用水中含100 mg/L硝酸钠）。通过腹腔注射STZ（60 mg/kg）诱导糖尿病。在确认糖尿病后立即进行所有干预，持续60天。在糖尿病诱导前和确认糖尿病后，通过热板试验、von Frey试验和尾撤离试验测量热痛觉和机械痛觉阈值。实验结束时，评估血清氧化氮水平和血清胰岛素水平。在实验开始时和实验期间记录血糖浓度和体重。
糖尿病大鼠出现痛觉减退、痛觉过敏以及感觉异常。与对照组大鼠相比，糖尿病大鼠表现出显著变化，包括尾撤离潜伏期缩短（第30天）、机械阈值降低（第60天）以及热板潜伏期延长（第61天）。硝酸盐和胰岛素预处理对糖尿病诱导的周围神经病变产生了保护作用。数据分析还显示，糖尿病大鼠的血糖水平显著升高，血清胰岛素和体重显著降低，而胰岛素和硝酸盐预处理均可使其恢复。
硝酸钠预处理对糖尿病神经病变具有保护作用，这可能是通过其降血糖作用和提高血清胰岛素水平介导的。
