| 彭影 朱雨岚 陈莉 刘羽 郭朝晖.1 5-HETE 参与的脑缺血再灌注损伤中 p-ERK1 /2 表达变化的研究[J].现代生物医学进展英文版,2014,14(35):6855-6858. |
| 1 5-HETE 参与的脑缺血再灌注损伤中 p-ERK1 /2 表达变化的研究 |
| Expression and Role of p-ERK in the Rats of 15-HETE-involvedCerebral Ischemia Reperfusion |
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| DOI： |
| 中文关键词: 去甲二氢愈创木酸 15- 羟基 - 二十碳四烯酸 15- 脂氧化酶 细胞外信号调节酶 脑缺血再灌注损伤 |
| 英文关键词: Nordihydroguaiaretic Acid 15-hydroxyeicosatetraenoic acid 15-Lipoxygenase Extracellular signal-regulated kinase Cerebral Ischemia Reperfusion |
| 基金项目:国家自 然科学基金项目（ 811 71077） |
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| 中文摘要: |
| 目 的： 通过应用 1 5- 脂氧化酶(1 5-Lipoxygenase， 15-LOX)抑制 剂 去甲二氢愈创 木酸(nordihydroguaiaretic acid， NDGA)抑制
15- 羟基 - 二十碳四烯酸(15-hydroxyeicosatetraenoic acid， 1 5-HETE)的生成， 观察缺血再灌注损伤中大鼠脑组织磷酸化细胞外信号
调节酶(phosphor-extracellular signal-regulated kinase， p-ERK1/2)表达的 变化， 探讨 p-ERK1 /2 在 15-HETE 参与 的 脑缺血再灌注损
伤中的作用 及其表达变化。 方法： 应用 大脑中动脉线栓栓塞法(MCAO)制 作大鼠脑梗死 2 小时再灌注模型。将大鼠随机分为三
组： 假手术组(sham 组)、DMSO 对照组、 NDGA 处理组。 后两组再根据不同 的灌注时间 分为三个亚组： 再灌注 1 小时组、再灌注 6
小时组、再灌注 24 小时组。 采用 TTC 染色法检测再灌注 24 小时大鼠脑梗死体积； 免疫印迹(Western blot)法测定梗死后再灌注不
同 时间点梗死核心区和梗死周围区的 p-ERK1 /2 的表达。 结果： 假手术组仅有少量 p-ERK1/2 的表达。 DMSO 对照组梗死核心区
p-ERK1 /2 的表达从梗死再灌注后 1 小时即开始逐渐升高 (1.43± 0.06)， 6 小时达高峰(2.02± 0.14)， 24 小时有所下降(1 .16± 0.21 ),
与 假手术组(0.62± 0.08)比较 P 值均 <0.01；梗死周围区 p-ERK1 /2 表现出 相同 的变化趋势。 与 DMSO 对照组比较， NDGA 处理组
大鼠脑梗死体积显著减小(20.10± 0.1 2 % vs 17.24± 0.1 6 %， P=0.009， P <0.05)， 各时间 点 p-ERK1/2 的表达均下降。 与 梗死核心区
相比较， 梗死周围区 24 小时仍可检测到较高含量的 p-ERK1/2(1 .16± 0.21 vs 1.86± 0. 1 4)， 但梗死核心区表达相对较少。 结论： 脑
缺血再灌注损伤中， p-ERK1 /2 的表达增加，说明 p-ERK1 /2 参与 其中； 应用 NDGA 后， p-ERK1/2 的表达降低， 脑梗死体积减小， 证
实 p-ERK1/2 参与 了 1 5-HETE 介导的脑缺血再灌注损伤， 并在此过程中可能参与 了 细胞的凋亡。 |
| 英文摘要: |
| Objective:To investigate the expression of phosphor-extracellular signal-regulated kinase p-ERK1 /2 in the rats of
15-HETE-invovled cerebral ischemia reperfusion (IR) by using NDGA, an inhibitor of 1 5-LOX and its role.Methods:The rats models of
middle cerebral artery occlusion (MCAO) were established and reperfused with introducing a nylon suture to the right internal carotid
artery. The rats were randomly divided into three groups: the sham operation group, the ischemia-reperfusion group and NDGA group.
According to different time points after IR, the animals were designated as subgroups 1h, 6h and 24h.The cerebral infarction volume was
measured by TTC staining. The content of p-ERK1/2 detected by Western blot analyses.Results:A few of p-ERK1/2 were expressed in
the sham group. Compared with the sham group, the expressions of the p-ERK1 /2 in the DMSO group began to increase at 1 h after
reperfusion, reach a peak at 6 h, and descend at 24 h. Compared with the DMSO group, the cerebral infarction volume was significantly
reduced and the contents of the p-ERK1/2 were decreased in each time group. The contents of p-ERK1 /2 at 24h in the infarction core
area were higher than that of the ischemic penumbra.Conclusion:The expressions of the p-ERK1 /2 increased on the rats of cerebral
ischemia reperfusion and decreased by the inhibitor NDGA through the 15-HETE pathway, which suggested that p-ERK1 /2 might be
involved in the cerebral ischemia reperfusion injury, and p-ERK1 /2 in this pathway might be also involved in apoptosis. |
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