Turkoglu Erhan, Serbes Gökhan, Dolgun Habibullah, Oztuna Sinem, Bagdatoglu Ozlen T, Yilmaz Necat, Bagdatoglu Celal, Sekerci Zeki
Ministry of Health Diskapi Yildirim Beyazit Research and Educational Hospital 1 Neurosurgery Clinic, 06610, Ankara, Turkey.
Surg Neurol Int. 2012;3:74. doi: 10.4103/2152-7806.98501. Epub 2012 Jul 14.
Ischemia/reperfusion (I/R) causes the production of toxic free radicals and leads to pathological changes in nerve tissue. We investigated the effect of alpha-melanocyte stimulating hormone (α-MSH) in a rat model for sciatic nerve I/R and discuss the possible cytoprotective and antioxidant mechanism of α-MSH against ischemic fiber degeneration.
Experiments were performed using 42 adult male Wistar rats. Rats were divided into six experimental groups: control group, ischemia group, I/R groups, and α-MSH treated groups. Ischemia was produced by clamping of the femoral vessels. Immediately after ischemia that lasted 3 h, 75 μg/kg of α-MSH was administered subcutaneously before reperfusion and the tissue malondialdehyde (MDA) level was evaluated as an indicator of lipid peroxidation in groups with different reperfusion periods.
The reperfusion injury did not begin in the first hour of reperfusion after 3 h of ischemia, and MDA levels increased on the first day of reperfusion. During the first day, blood MDA levels were decreased in the α-MSH group compared to the control group. The tissue from animals pre-treated with α-MSH showed fewer morphological alterations. Myelin breakdown was significantly diminished after treatment with α-MSH, and the ultrastructural features of axons showed remarkable improvement. Two-way analysis of variance was used for comparing three or more groups. When a significant difference existed, the post-hoc multiple-comparison test was applied to demonstrate the differences.
The results confirm that pre-treatment with α-MSH after ischemia protected the peripheral nerves against I/R injury.
缺血/再灌注(I/R)会导致有毒自由基的产生,并引发神经组织的病理变化。我们在大鼠坐骨神经I/R模型中研究了α-黑素细胞刺激素(α-MSH)的作用,并探讨了α-MSH对缺血性纤维变性可能的细胞保护和抗氧化机制。
使用42只成年雄性Wistar大鼠进行实验。大鼠被分为六个实验组:对照组、缺血组、I/R组和α-MSH治疗组。通过夹闭股血管造成缺血。在持续3小时的缺血后立即进行再灌注,在再灌注前皮下注射75μg/kg的α-MSH,并将组织丙二醛(MDA)水平作为不同再灌注期脂质过氧化的指标进行评估。
缺血3小时后,再灌注损伤在再灌注的第一小时并未开始,且MDA水平在再灌注第一天升高。在第一天,与对照组相比,α-MSH组的血液MDA水平降低。用α-MSH预处理的动物组织形态学改变较少。用α-MSH治疗后髓鞘破坏明显减轻,轴突的超微结构特征有显著改善。采用双向方差分析比较三组或更多组。当存在显著差异时,应用事后多重比较检验来证明差异。
结果证实缺血后用α-MSH预处理可保护周围神经免受I/R损伤。