关键词: cholinergic neuron cilostazol diabetic rat motor neuron neuropathy schwannopathy

Mesh : Animals Cilostazol / pharmacology therapeutic use Schwann Cells / drug effects metabolism Diabetes Mellitus, Experimental / drug therapy metabolism Rats Male Sciatic Nerve / drug effects metabolism Choline O-Acetyltransferase / metabolism Rats, Sprague-Dawley Spinal Cord / drug effects metabolism Motor Neurons / drug effects metabolism Glial Fibrillary Acidic Protein / metabolism Myelin P0 Protein / metabolism Streptozocin

来  源:   DOI:10.3390/ijms25147847   PDF(Pubmed)

Abstract:
This study investigated the effects of cilostazol on motor dysfunction, spinal motor neuron abnormalities, and schwannopathy in rats with diabetes. Diabetes mellitus (DM) was induced in rats via femoral intravenous streptozotocin (STZ) injection (60 mg/kg). After successful DM induction, cilostazol was administered on day 15 via oral gavage (100 mg/kg/day) for 6 weeks until sacrifice. Behavioral assays, including motor function, were performed weekly. The sciatic nerve, L5 spinal cord, and spinal ventral root were collected to evaluate the expression of the glial fibrillary acidic protein (GFAP), myelin protein zero (P0), and choline acetyltransferase (ChAT) by immunofluorescence and Western blotting. DM rats displayed decreased running speeds, running distances, and toe spread but increased foot pressure. In addition, loss of non-myelinating Schwann cells and myelin sheaths was observed in the sciatic nerve and L5 spinal ventral root. Reduced numbers of motor neurons were also found in the L5 spinal ventral horn. Cilostazol administration significantly potentiated running speed and distance; increased hind paw toe spread; and decreased foot pressure. In the sciatic nerve and L5 spinal ventral root, cilostazol treatment significantly improved non-myelinated Schwann cells and increased myelin mass. ChAT expression in motor neurons in the spinal ventral horn was improved, but not significantly. Cilostazol administration may protect sensorimotor function in diabetic rats.
摘要:
这项研究调查了西洛他唑对运动功能障碍的影响,脊髓运动神经元异常,和糖尿病大鼠的schwannopathy。通过股静脉内链脲佐菌素(STZ)注射(60mg/kg)在大鼠中诱发糖尿病(DM)。DM诱导成功后,在第15天通过口服管饲法(100mg/kg/天)施用西洛他唑6周直至处死。行为分析,包括运动功能,每周进行一次。坐骨神经,L5脊髓,收集脊髓腹根,评估胶质纤维酸性蛋白(GFAP)的表达,髓磷脂蛋白零(P0),和胆碱乙酰转移酶(ChAT)通过免疫荧光和蛋白质印迹。DM大鼠表现出跑步速度下降,跑步距离,脚趾伸展,但增加了脚的压力。此外,在坐骨神经和L5脊髓腹根中观察到非髓鞘化雪旺氏细胞和髓鞘的丢失。在L5脊髓腹角中也发现运动神经元数量减少。西洛他唑的使用显着增强了跑步速度和距离;增加了后爪脚趾的伸展;并降低了脚部压力。在坐骨神经和L5脊髓腹根,西洛他唑治疗可显着改善非髓鞘施万细胞并增加髓鞘质量。脊髓腹角运动神经元中ChAT的表达得到改善,但不是很重要。西洛他唑可保护糖尿病大鼠的感觉运动功能。
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