Department of Pharmacology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Neuroscience Unit, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
J Diabetes Res. 2021 Jan 16;2021:6927025. doi: 10.1155/2021/6927025. eCollection 2021.
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 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 M). 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 model. This could be through carvedilol antioxidant effects.
糖尿病周围神经病变是全球糖尿病患者的主要并发症。使用有效的治疗方法对于减少糖尿病患者的健康并发症至关重要。本研究评估了卡维地洛对糖尿病周围神经病变的潜在神经保护作用。使用糖尿病周围神经病变模型,包括从小鼠 C57BL 的背根神经节 (DRG) 培养的细胞。这些细胞在高葡萄糖 (HG) 培养基 (45mM) 中培养约二十四小时。一些细胞用卡维地洛 (10μM) 孵育。测量神经元活力、神经元形态和激活转录因子 3 (AFT3)。HG 培养基降低了细胞活力,同时也降低了神经元长度、胞体面积和胞体周长。此外,AFT3 的过度表达是神经元应激反应的标志物。与 HG 处理的细胞相比,卡维地洛预处理增加了 DRG 的活力。同时,它显著保护 DRG 免受 HG 诱导的形态变化。尽管 AFT3 的表达有所下降,但统计学结果并不显著。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。这可能是通过卡维地洛的抗氧化作用。