远程缺血后处理对大鼠局灶性脑缺血神经保护作用的研究

发布时间：2018-08-26 18:13

【摘要】：目的:探讨远程缺血后处理(Remote ischemic postconditioning,RIPC)对SD大鼠局灶性脑缺血模型的长期神经保护作用。方法:60只SPF级健康雄性SD大鼠随机分为Sham(Sham operation)组、MCAO(Cerebral ischemic occlusion)组、R-RIPC(Rapid-RIPC)组和D-RIPC(Delayed-RIPC)组,每组15只实验大鼠。除Sham组,其余各组大鼠均使用Longa改良线栓法制备局灶性大脑中动脉缺血(MCAO)模型。Sham组(n=15):即假手术组,15只健康雄性SD实验大鼠手术过程同MCAO组,但不做局灶性脑缺血处理;MCAO组(n=15):即缺血对照组,本组15只健康雄性SD实验大鼠全部为90min局灶性大脑中动脉缺血模型;R-RIPC组(n=15):即快速性RIPC组,15只健康雄性SD实验大鼠于90min局灶性大脑中动脉缺血再灌注后即刻进行RIPC,即分离实验大鼠双侧股动脉(Bilateral com femoral artery,BCFA),给予BCFA 5min短暂性非损伤性缺血处理,间歇再灌注5min,以每个短暂性缺血再灌注为一个循环,共进行4个缺血再灌注循环,总计40min RIPC;D-RIPC组(n=15):即延迟性RIPC,15只健康雄性SD实验大鼠于90min局灶性大脑中动脉缺血再灌注后6h进行RIPC,处理方式同R-RIPC组。各组实验大鼠术后均进行旋转棒法运动性神经功能检测和粘胶法感觉性神经功能检测,检测时间为缺血再灌注后1d、7d、14d、21d与28d。全部四组实验大鼠于再灌注第30d使用4%多聚甲醛灌注取脑,并进行组织病理学检测。结果:1、脑梗死检测:mcao组、d-ripc组与r-ripc组脑梗死面积百分比分别为(94.05±3.82)%,(89.73±3.45)%,(91.7±4.59)%。相对于sham组,mcao组、d-ripc组与r-ripc组实验大鼠脑梗死损伤严重(p0.05)。相对于mcao组,r-ripc组的脑梗死面积仅减少4.32%(p0.05);d-ripc组与mcao组以及d-ripc组与r-ripc组的脑梗死面积未见明显差异(p0.05)。2、运动功能检测:①相对于sham组,局灶性缺血再灌注后1d-14d,mcao组、d-ripc组、r-ripc组运动神经功能损伤严重(p0.05);局灶性缺血再灌注后21d-28d,mcao组、r-ripc组与sham组有显著差异(p0.05),sham组与d-ripc组之间运动功能缺损程度无显著差异(p0.05)。②与mcao组相比较,局灶性缺血再灌注后1d,mcao组、d-ripc组、r-ripc组运动神经功能缺损程度无差异(p0.05);局灶性缺血再灌注后7d-21d,mcao组与r-ripc组运动神经功能评分无显著差异(p0.05);局灶性缺血再灌注后28d,mcao组与r-ripc组运动神经功能具有显著差异(p0.05);局灶性缺血再灌注后7d-28d,mcao组与d-ripc组存在显著差异(p0.05)。③d-ripc组、r-ripc组运动神经功能检测结果显示,局灶性缺血再灌注后1d-7d,r-ripc组与d-ripc组运动神经功能检测无显著差异(p0.05);局灶性缺血再灌注后14d-28d,r-ripc组与d-ripc组运动神经功能检测存在显著差异(p0.05)。3、感觉功能检测:①相对于sham组,局灶性缺血再灌注后1d-7d,mcao组、r-ripc组与d-ripc组与sham组感觉神经功能检测均无显著差异(p0.05);局灶性缺血再灌注后14d,sham组与r-ripc组大鼠粘胶刺激强度存在显著差异(p0.05),d-ripc组与sham组感觉神经功能检测均无显著差异(p0.05)。②与mcao组相比较,局灶性缺血再灌注后1d,mcao组与r-ripc组感觉性神经功能检测无差异(p0.05);局灶性缺血再灌注后28d,MCAO组与R-RIPC组感觉性神经功能检测存在显著差异(P0.05);局灶性缺血再灌注后1d-28d,D-RIPC组感觉性神经功能评分明显低于MCAO组(P0.05)。③D-RIPC组、R-RIPC组感觉性神经功能检测结果显示,只有局灶性缺血再灌注后7d,R-RIPC组与D-RIPC组感觉性神经功能检测存在显著差异(P0.05)。结论:RIPC对SD实验大鼠局灶性脑缺血损伤具有的神经保护作用,尤其是延迟性RIPC,对于局灶性缺血模型的运动以及感觉功能的恢复具有持久的保护效果。
[Abstract]:Objective: To investigate the long-term neuroprotective effects of remote ischemic postconditioning (RIPC) on focal cerebral ischemia in SD rats. Methods: Sixty SPF-grade healthy male SD rats were randomly divided into Sham operation group, MCAO (Cerebral ischemic occlusion) group, R-RIPC (Rapid-RIPC) group and D-RIPC (Delayed-RIPC) group, each group. The sham group (n = 15): sham operation group, 15 healthy male SD experimental rats were operated on in the same way as the MCAO group, but without focal cerebral ischemia treatment; MCAO group (n = 15): ischemic control group, 15 healthy male. All the SD rats were focal middle cerebral artery ischemia model for 90 minutes; R-RIPC group (n=15): Fast RIPC group, 15 healthy male SD rats were given RIPC immediately after 90 minutes of focal middle cerebral artery ischemia-reperfusion, that is, bilateral femoral artery (BCFA) was separated and BCFA was given for 5 minutes. Non-invasive ischemia, intermittent reperfusion for 5 minutes, with each transient ischemia-reperfusion as a cycle, a total of 4 ischemia-reperfusion cycles, a total of 40 minutes RIPC; D-RIPC group (n=15): that is, delayed RIPC, 15 healthy male SD experimental rats in 90 minutes after focal middle cerebral artery ischemia-reperfusion 6 hours RIPC, the same treatment as the R-RIPC group. All the four groups of rats were perfused with 4% paraformaldehyde on the 30th day after reperfusion, and the brain tissues were examined by histopathology. Results: 1. Cerebral infarction detection: MCA The percentage of cerebral infarction area in group o, d-ripc and r-ripc was (94.05 (+) 3.82)% (89.73 (+) 3.45)% (91.7 (+) 4.59)%. compared with sham group, the cerebral infarction area in d-ripc group and r-ripc group was severely damaged (p0.05). compared with MCAO group, the cerebral infarction area in r-ripc group was only reduced by 4.32% (p0.05). There was no significant difference in the area of cerebral infarction (p0.05). 2. motor function test: compared with sham group, 1-14 days after focal ischemia-reperfusion, MCAO group, d-ripc group, r-ripc group, motor nerve function injury was serious (p0.05); 21-28 days after focal ischemia-reperfusion, MCAO group, r-ripc group and sham group were significantly different (p0.05), sham group and d-ripc group were significantly different (p0.05). There was no significant difference in the degree of motor function impairment between MCAO group and r-ripc group (p0.05). The motor nerve function of MCAO group and r-ripc group was significantly different (p0.05) on the 28th day after focal ischemia-reperfusion, and there was significant difference between MCAO group and d-ripc group (p0.05) on the 7th-28th day after focal ischemia-reperfusion. There was significant difference in motor nerve function between r-ripc group and d-ripc group at 14-28 days after focal ischemia-reperfusion (p0.05). 14 days after perfusion, there was significant difference in the viscose stimulation intensity between sham group and r-ripc group (p0.05). There was no significant difference in sensory nerve function between d-ripc group and sham group (p0.05). 2 Compared with MCAO group, there was no difference in sensory nerve function between MCAO group and r-ripc group at 1 day after focal ischemia-reperfusion (p0.05). There was significant difference in sensory nerve function between CAO group and R-RIPC group (P 0.05); sensory nerve function score of D-RIPC group was significantly lower than that of MCAO group (P 0.05) 1-28 days after focal ischemia-reperfusion (P 0.05). Conclusion: RIPC has neuroprotective effect on focal cerebral ischemia injury in SD rats, especially delayed RIPC, which has a lasting protective effect on motor and sensory function recovery of focal cerebral ischemia model.
【学位授予单位】：桂林医学院
【学位级别】：硕士
【学位授予年份】：2015
【分类号】：R743.33

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