PDF(Pubmed)
Abstract：
Diabetic neuropathy serves as a major complication for diabetic patients across the world. The use of effective treatment is integral for reducing the health complications for diabetic patients. This study has evaluated the carvedilol potential neuroprotective effect on diabetic neuropathy. An in vitro model of diabetic neuropathy was used, including dorsal root ganglia (DRG) that were cultured from male adult mice C57BL. These were incubated for about twenty-four hours in high glucose (HG) media (45 mM). Some cells were incubated with carvedilol (10 μM). Neuronal viability, neuronal morphology, and activating transcription factor 3 (AFT3) were measured. The cell viability was decreased, along with neuronal length, soma area, and soma perimeter with HG media. Also, there was an overexpression of ATF3, which is a neuronal stress response marker. The pretreatment with carvedilol increased the viability of DRG as compared to HG-treated cells. Also, it significantly protected the DRG from HG-induced morphology changes. Though it shows a decrease in AFT3 expression, the statistical results were insignificant. The current study demonstrates the neuroprotective effect of carvedilol against HG-induced DN using an in vitro model. This could be through carvedilol antioxidant effects.
摘要：
糖尿病性神经病是全世界糖尿病患者的主要并发症。使用有效的治疗对于减少糖尿病患者的健康并发症是不可或缺的。这项研究评估了卡维地洛对糖尿病神经病变的潜在神经保护作用。使用糖尿病神经病变的体外模型，包括从雄性成年小鼠C57BL培养的背根神经节（DRG）。将这些在高葡萄糖(HG)培养基(45mM)中孵育约24小时。将一些细胞与卡维地洛(10μM)孵育。神经元活力,神经元形态学，和激活转录因子3（AFT3）进行测量。细胞活力下降，随着神经元的长度，躯体区,和带有HG培养基的躯体周长。此外，ATF3是一种神经元应激反应标志物。与HG处理的细胞相比,卡维地洛预处理增加了DRG的活力。此外，它显著保护DRG免受HG诱导的形态变化。虽然它显示AFT3表达减少，统计结果不显著。本研究使用体外模型证明了卡维地洛对HG诱导的DN的神经保护作用。这可以通过卡维地洛的抗氧化作用来实现。
