Prostaglandin E1 reduces compression trauma-induced spinal cord injury in rats mainly by inhibiting neutrophil activation
Prostaglandin E1 reduces compression trauma-induced spinal cord injury in rats mainly by inhibiting neutrophil activation
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DOI：
10.1089/08977150360547125
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发表时间：
2003-02-01
影响因子：
4.2
通讯作者：
Takagi, K
中科院分区：
文献类型：
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作者：
Naruo, S;Okajima, K;Takagi, K
前列腺素E-1 (PGE(1))，一种有效的血管扩张剂，最近被报道在体外抑制中性粒细胞激活和单核细胞产生肿瘤坏死因子- α (tnf - α)。我们之前报道过，tnf - α通过增加压迫性创伤性脊髓损伤大鼠损伤部位中性粒细胞的积累，在运动障碍的发展中起关键作用。因此，PGEI可能通过抑制脊髓损伤大鼠的中性粒细胞激活来减轻运动障碍。我们在大鼠脊髓损伤（SCI）模型中检验了这种可能性。使用斜面试验和足迹分析评估脊髓压迫引起的运动障碍。通过测量组织髓过氧化物酶（MPO）活性来评估创伤部位中性粒细胞的积累。使用酶联免疫吸附法测定组织中tnf - α的水平。大鼠给予PGE后，脊髓压迫引起的运动障碍明显减轻(1)。组织学检查显示，创伤后24小时观察到的髓内出血在给予PGE的动物中明显减少(1)。在接受PGE治疗的动物中，受损脊髓段的组织中tnf - α水平和MPO活性的增加明显受到抑制(1)。这些观察结果表明，PGE(1)通过直接或间接抑制损伤部位tnf - α的产生，抑制中性粒细胞的激活，从而减轻运动障碍。PGE(1)的这些作用可能至少在一定程度上有助于大鼠脊髓损伤的治疗作用。
Prostaglandin E-1 (PGE(1)), a potent vasodilator, was recently reported to inhibit both neutrophil activation and monocytic production of tumor necrosis factor-alpha (TNF-alpha) in vitro. We previously reported that TNF-alpha was critically involved in the development of motor disturbances by increasing the accumulation of neutrophils at the site of injury in rats subjected to compression trauma-induced spinal cord injury. Therefore, it is possible that PGEI reduces motor disturbances by inhibiting neutrophil activation in rats subjected to spinal cord injury. We examined this possibility in a rat model of spinal cord injury (SCI). Motor disturbances induced by spinal cord compression were evaluated using the inclined plane test, and footprint analysis. Accumulation of neutrophils at the site of trauma was evaluated by measuring tissue myeloperoxydase (MPO) activity. Tissue levels of TNF-alpha were determined using an enzyme-linked immunosorbent assay. Motor disturbances induced by spinal cord compression were significantly attenuated in rats administered PGE(1). A histological examination revealed that intramedullary hemorrhages, observed 24 h after trauma, were markedly reduced in animals administered PGE(1). Increases in the tissue levels of TNF-alpha and MPO activity in the damaged segment of spinal cord were significantly inhibited in animals that had received PGE(1). These observations suggested that PGE(1) reduces motor disturbances by inhibiting neutrophil activation directly or indirectly through the inhibition of TNF-alpha production at the site of injury. These effects of PGE(1) might at least partly contribute to therapeutic effect on SCI in rats.