Schwann cell is a target in ischemia-reperfusion injury to peripheral nerve
Schwann cell is a target in ischemia-reperfusion injury to peripheral nerve
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DOI：
10.1002/mus.20159
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发表时间：
2004-12-01
期刊：
影响因子：
3.4
通讯作者：
Low, PA
中科院分区：
文献类型：
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作者：
Ilda, H;Schmeichel, AM;Low, PA
缺血再灌注（IR）由于神经元和轴突的损伤，引起氧化损伤和缺血性纤维变性。在这项研究中，我们利用我们建立的大鼠IR损伤模型，探讨氧化应激对雪旺细胞的影响，雪旺细胞是一个特定的周围神经靶点。实验用了56只大鼠。6组（N = 8）后肢完全缺血4 h，再灌注时间分别为0 h、3 h、7 d、14 d、28 d、42 d。1组行假手术（N = 8）。我们使用抗8-羟基脱氧鸟苷（8-OHdG）评估免疫组织化学标记对氧化损伤的影响。为了鉴定凋亡的细胞，我们研究了caspase-3和末端脱氧核苷酸转移酶（TdT）介导的dutp -生物素缺口末端标记（TUNEL）阳性的免疫标记。在假手术组、0-h组和3-h组仅见最低的阳性反应。再灌注时间较长的组（8-OHdG， 7-28天；caspase-3, 14-42天；TUNEL， 14-42天）8-OHdG、caspase-3和TUNEL的阳性均显著升高。轴突周围的阳性细胞通过其形态和与S-100的标记鉴定为雪旺细胞。我们得出结论，雪旺细胞凋亡发生在再灌注过程中，即使轴突再生也会继续。雪旺细胞凋亡可导致轴突功能和纤维再生效率受损。已知这两种异常都发生在实验和人类糖尿病神经中。
Ischemia-reperfusion (IR) causes oxidative injury and ischemic fiber degeneration due to injury of the neuron and axon. In this study, we explore the effect of oxidative stress on Schwann cells, as a specific peripheral nerve target, using our established rat model for IR injury. Fifty-six rats were used. Six groups (N = 8 each) underwent complete hindlimb ischemia for 4 It, followed by reperfusion durations of 0 h, 3 h, 7 days, 14 days, 28 days, and 42 days. One group underwent sham operation (N = 8). We evaluated immunohistochemical labeling for oxidative injury using anti-8-hydroxydeoxyguanosine (8-OHdG). To identify cells committed to apoptosis, we studied immunolabeling to caspase-3 and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL) positivity. Only minimal positivity was seen in the sham, 0-h, and 3-h groups. Positivity to 8-OHdG, caspase-3, and TUNEL increased significantly in groups undergoing longer reperfusion (8-OHdG, 7-28 days; caspase-3, 14-42 days; TUNEL, 14-42 days). The positive cells surrounding axons were identified as being Schwann cells by their configuration and colabeling with S-100. We conclude that apoptosis of Schwann cells occurs during reperfusion and continues even when axons regenerate. Schwann cell apoptosis could contribute to impairment of axonal function and efficiency of fiber regeneration. Both these abnormalities are known to occur in experimental and human diabetic nerves.