Department of Orthopedics, Second Affiliated Hospital of Medicine School of Xi'an Jiaotong University, Xi'an Shaanxi, China.
J Vasc Surg. 2011 Jul;54(1):192-200. doi: 10.1016/j.jvs.2010.12.030. Epub 2011 Mar 31.
Inflammation, which is known to be detrimental to the neurologic outcome during the acute phase after an ischemic stroke, provides a potential target for preventive or therapeutic approach for spinal cord ischemia-reperfusion injury. Tetramethylpyrazine (TMP), a pure compound derived from Ligusticum chuanxiong, is widely used in the treatment of ischemic stroke. The present study aimed to gain a deeper insight into the mechanism underlying the anti-inflammatory effects of TMP on spinal cord ischemia-reperfusion injury.
Spinal cord ischemia was induced in male Sprague-Dawley rats by balloon occlusion of the thoracic aorta. The experimental groups (n = 30 per group) included sham operation, control (receiving only normal saline), and TMP (30 mg/kg, 30 minutes before occlusion). Neurologic function was assessed by the Basso, Beattie, and Bresnahan (BBB) score at 1, 6, 12, 24, and 48 hours after reperfusion. Histologic changes were studied using Nissl staining. Infarct volume was analyzed using 2,3,5-triphenyltetrazolium chloride staining. Myeloperoxidase (MPO) activity was determined by using a rat MPO assay kit. Interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-10 and nuclear factor (NF)-κB were examined with immunohistochemistry, enzyme-linked immunosorbent assay (ELISA) and Western blotting.
Compared with the control group, the TMP group showed significantly improved neurologic outcome (P < .05), decreased infarct volume (42.3% vs 17.4%), and alleviated neutrophil infiltration (0.35 vs 0.18 U/g). TMP treatment reduced the expressions of proinflammatory cytokines TNF-α (28.62 vs 15.23 pg/mg protein) and IL-1β (13.62 vs 8.24 pg/mg protein), upregulated the expression of anti-inflammatory cytokine IL-10 (18.35 vs 31.26 pg/mg protein), and inhibited the activation of NF-κB (2.78 vs 1.22) in ischemic spinal cord.
Treatment with TMP exerted a neuroprotective effect against spinal cord ischemia-reperfusion injury. The anti-inflammatory effect was believed to be one of the contributing mechanisms.
炎症已知会对缺血性中风后急性期的神经功能预后产生不利影响，为脊髓缺血再灌注损伤的预防或治疗方法提供了一个潜在的靶点。川芎嗪（TMP）是一种从川芎中提取的纯化合物，广泛用于治疗缺血性中风。本研究旨在更深入地了解 TMP 对脊髓缺血再灌注损伤的抗炎作用机制。
通过气囊阻塞胸主动脉诱导雄性 Sprague-Dawley 大鼠脊髓缺血。实验组（每组 n = 30）包括假手术、对照（仅接受生理盐水）和 TMP（再灌注前 30 分钟给予 30mg/kg）。再灌注后 1、6、12、24 和 48 小时通过 Basso、Beattie 和 Bresnahan（BBB）评分评估神经功能。使用尼氏染色研究组织学变化。通过 2,3,5-三苯基氯化四唑染色分析梗死体积。通过大鼠 MPO 测定试剂盒测定髓过氧化物酶（MPO）活性。用免疫组化、酶联免疫吸附试验（ELISA）和 Western blot 检测白细胞介素（IL）-1β、肿瘤坏死因子（TNF）-α、IL-10 和核因子（NF）-κB。
与对照组相比，TMP 组的神经功能明显改善（P <.05），梗死体积减少（42.3%对 17.4%），中性粒细胞浸润减轻（0.35 对 0.18 U/g）。TMP 治疗降低了促炎细胞因子 TNF-α（28.62 对 15.23 pg/mg 蛋白）和 IL-1β（13.62 对 8.24 pg/mg 蛋白）的表达，上调了抗炎细胞因子 IL-10（18.35 对 31.26 pg/mg 蛋白）的表达，并抑制了缺血性脊髓中 NF-κB 的激活（2.78 对 1.22）。
TMP 治疗对脊髓缺血再灌注损伤具有神经保护作用。抗炎作用被认为是其中的一种机制。
