[1]吴光勇,李亮,廖达光,等.Apelin-13对大鼠局灶性脑缺血-再灌注损伤的保护作用[J].南方医科大学学报,2015,(09):1335.
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Apelin-13对大鼠局灶性脑缺血-再灌注损伤的保护作用(/HTML)
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《南方医科大学学报》[ISSN:/CN:]

卷:
期数:
2015年09期
页码:
1335
栏目:
出版日期:
2015-09-15

文章信息/Info

Title:
Protective effect of Apelin-13 on focal cerebral ischemia-reperfusion injury in rats
作者:
吴光勇李亮廖达光王知非
关键词:
Apelin-13脑缺血-再灌注损伤MDASODERK1/2
Keywords:
apelin-13 brain ischemia-reperfusion injury malondialdehyde superoxide dismutase extracellular regulatedkinase1/2
摘要:
目的探讨Apelin-13对大鼠局灶性脑缺血-再灌注损伤(CIRI)的保护作用及其可能的机制。方法改良线栓法建立S-D大
鼠局灶性CIRI模型,分假手术组、模型组、小剂量Apelin-13干预A组、中剂量B组、大剂量C组共5组,Apelin-13进行侧脑室注
射,分别进行神经功能评分,脑水肿、脑梗死体积测定,观察细胞凋亡;检测脑组织丙二醛(MDA)、超氧化物歧化酶(SOD)的活
性和细胞外调节蛋白激酶1/2(ERK1/2)。结果(1)B、C组较模型组神经功能评分降低(P<0.05),含水量、脑梗死体积降低(P<
0.05);模型组梗死组织可见水肿、坏死,较多深染、固缩核细胞;B组、C组TUNEL阳性细胞数低于模型组(P<0.05);(2)B、C组
缺血周边脑组织MDA含量降低,SOD的活性增加(P<0.05);(3)各组ERK1/2 蛋白表达无差异性(P>0.05);模型组和干预组
p-ERK1/2蛋白表达高于假手术组(P<0.05);干预组高于模型组(P<0.05)。结论Apelin-13可能通过抑制氧化应激反应对大鼠
局灶性CIRI起保护作用;ERK1/2信号通路可能参与了Apelin-13保护作用机制。
Abstract:
Objective To investigate the protective effect of Apelin-13 on focal cerebral ischemia-reperfusion injury in rats.
Methods Focal transient cerebral ischemia-reperfusion injury was induced in male SD rats using modified suture occlusion
technique. The rats were randomly divided into 5 groups: Sham group, Model group, Apelin-low dose (A) group,
Apelin-middle dose (B) group and Apelin-high dose (C) group. Apelin-13 was injected into lateral cerebral ventricle, and the
neurological function score, brain edema, infarct volume, apoptosis, malondialdehyde (MDA), superoxide dismutase (SOD)
and extracellular regulated kinase1/2 (ERK1/2) protein were measured. Results Neurological function scores, percentage of
brain water content, infarct volumes and TUNEL-positive cells in B and C groups were lower than those in Model group (P<
0.05). The level of MDA in the tissue bomogenate of brain tissue in the surrounding area of ischemia of B and C groups was
lower than that of Model group, while the activity of SOD was higher (P<0.05). There was no significant difference in ERK1/2
protein expression among the groups (P>0.05). P-ERK1/2 increased in Model group and A, B, and C groups compared with
Sham group (P<0.05), and that of A, B, and C group was higher than that of Model group (P<0.05). Conclusion Apelin-13 may
play an important role by inhibiting oxidative stress to protect against focal cerebral ischemia-reperfusion injury; ERK1/2
signaling pathway may be involved in the protective mechanism of Apelin-13.
更新日期/Last Update: 1900-01-01