Rat Bone Marrow-Derived Mononuclear Cells Outperform Folic Acid in the Treatment of Diabetic Peripheral Neuropathy in Streptozotocin-Induced Diabetic Rats

Manal H Al-Badawi, Basma S. Abd El-Hay, S. A. Fareed, M. H. Mohamed
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Abstract

Background: Diabetes mellitus is the most common cause of peripheral neuropathy, which itself is mediated in part via oxidative stress. Recent studies have used stem-cell-based therapies to regenerate nerve tissues following diabetic neuropathy. Folic acid supplementation promotes neuronal development and protection in some neurological diseases. Aim: This study aims to compare the effects of bone marrow-mononuclear cells (BM-MNCs) and folic acid (FA) in the treatment of peripheral neuropathy in streptozotocin-induced diabetic rats. Methods: Forty adult male albino rats were randomly divided into five groups: Group I (healthy control group); Group II, diabetic group (a single intraperitoneal streptozotocin injection); Group III, diabetic rats that received BM-MNCs; Group IV, diabetic rats that were treated with FA (10 mg/kg/day intraperitoneal injection) for 4 weeks and Group V (FA): Folic Acid-treated group. Random blood sugar was measured for all groups. The animals were euthanized, and the right sciatic nerve was carefully extracted to measure sciatic nerve conduction velocity and processed for histopathological, immunohistochemical (CD68), electron microscopic and morphometric studies. Results: The diabetic group showed progressive histological changes characteristic of neuropathy in the sciatic nerve. Also increased number of CD68-immunopositive cells were detected. In BM-MNC transplantation group, the sciatic nerve sections showed improved histological changes characteristic of neuropathy with a decreased number of CD68-immunopositive cells. The diabetic group treated with FA showed less histological results relative to diabetic rats treated with BM-MNCs. Conclusion: Diabetic rats treated with BM-MNC showed better improvement in diabetic neuropathy than diabetic rats treated with folic acid.
大鼠骨髓来源的单核细胞在治疗链脲佐菌素诱导的糖尿病大鼠糖尿病周围神经病变方面优于叶酸
背景:糖尿病是周围神经病变最常见的原因,其本身部分是通过氧化应激介导的。最近的研究已经使用基于干细胞的疗法来再生糖尿病神经病变后的神经组织。叶酸补充促进神经发育和保护一些神经系统疾病。目的:比较骨髓单核细胞(BM-MNCs)和叶酸(FA)对链脲霉素诱导的糖尿病大鼠周围神经病变的治疗作用。方法:40只成年雄性白化病大鼠随机分为5组:ⅰ组(健康对照组);II组,糖尿病组(单次腹腔注射链脲佐菌素);第三组,糖尿病大鼠接受BM-MNCs治疗;四组:糖尿病大鼠给予FA (10 mg/kg/天腹腔注射)治疗4周;五组(FA):叶酸治疗组。随机测量各组的血糖。对大鼠实施安乐死后,仔细提取右侧坐骨神经,测定坐骨神经传导速度,并进行组织病理学、免疫组化(CD68)、电镜和形态计量学研究。结果:糖尿病组表现出以坐骨神经病变为特征的进行性组织学改变。同时检测到cd68免疫阳性细胞数量增加。BM-MNC移植组坐骨神经切片表现出神经病变特征的组织学改变,cd68免疫阳性细胞数量减少。与BM-MNCs治疗的糖尿病大鼠相比,FA治疗的糖尿病大鼠组织学结果更少。结论:BM-MNC对糖尿病大鼠糖尿病神经病变的改善作用优于叶酸。
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