Sherif Rania N
Department of Anatomy and Embryology, Faculty of Medicine, University of Mansoura, Mansoura, 35516, Egypt.
Tissue Cell. 2017 Dec;49(6):726-733. doi: 10.1016/j.tice.2017.10.006. Epub 2017 Oct 25.
Diabetes mellitus represents one of the disorders in the metabolism that affects all body systems including CNS. Cerebrolysin contains many neurotrophic factors, and many studies reported that it can be used treatment of many neurological disorders.
The aim of the current study was to study the potential neuroprotective effect of cerebrolysin on the cerebellum of diabetic rat.
Sprague Dawley male rats were divided randomly into four groups: control, cerebrolysin (Cbl), diabetes and diabetes treated with Cbl groups. Induction of diabetes was performed by intraperitoneal injection of 60mg/kg streptozotocin once. Eight weeks later, the rats were anaesthetized, sacrificed and the cerebellum was removed. Cerebellum oxidative stress markers were analysis. Cerebellar tissue was subjected to histolopathological examination and immune-histological assessment of GFAP and Synaptophysin.
As compared to the control group, diabetes caused degenerative changes in the cerebellum with significant elevation of MDA and decrease of SOD levels and gliosis confirmed by increase the GFAP expression area fraction. Diabetes increased significantly the optical density of synaptophysin expression with increase in its area fraction in the granular layer. Although Cbl treatment succeeded in minimizing the changes in the oxidative stress markers, it had no effect on pathological changes of the diabetic cerebellum. Cerebrolysin treatment of diabetic rats decreased the area fraction of GFAP positive immunoreactivity and had no effect on synaptophysin expression.
Cerebrolysin can potentially protect against diabetes induced changes in the cerebellum through minimizing the oxidative stress and improving the gliosis.
糖尿病是一种影响包括中枢神经系统在内的所有身体系统的代谢紊乱疾病。脑蛋白水解物含有多种神经营养因子，许多研究报道其可用于治疗多种神经系统疾病。
本研究旨在探讨脑蛋白水解物对糖尿病大鼠小脑的潜在神经保护作用。
将雄性Sprague Dawley大鼠随机分为四组：对照组、脑蛋白水解物组（Cbl）、糖尿病组和糖尿病脑蛋白水解物治疗组。通过腹腔注射60mg/kg链脲佐菌素诱导糖尿病一次。八周后，将大鼠麻醉、处死并取出小脑。分析小脑氧化应激标志物。对小脑组织进行组织病理学检查以及胶质纤维酸性蛋白（GFAP）和突触素的免疫组织学评估。
与对照组相比，糖尿病导致小脑发生退行性改变，丙二醛（MDA）显著升高，超氧化物歧化酶（SOD）水平降低，胶质细胞增生通过GFAP表达面积分数增加得以证实。糖尿病显著增加了突触素表达的光密度及其在颗粒层的面积分数。尽管脑蛋白水解物治疗成功地使氧化应激标志物的变化最小化，但对糖尿病小脑的病理变化没有影响。脑蛋白水解物治疗糖尿病大鼠降低了GFAP阳性免疫反应性的面积分数，对突触素表达没有影响。
脑蛋白水解物可通过最小化氧化应激和改善胶质细胞增生来潜在地预防糖尿病引起的小脑变化。
