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首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Preconditioning with +Gz acceleration (head-to-foot inertial load) produces neuroprotection against transient focal cerebral ischemia in rats.
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Preconditioning with +Gz acceleration (head-to-foot inertial load) produces neuroprotection against transient focal cerebral ischemia in rats.

机译:用+ Gz加速度(头到脚惯性负载)进行预处理可对大鼠短暂性局灶性脑缺血产生神经保护作用。

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摘要

Ischemic preconditioning is considered to be the most robust endogenous neuroprotectant. However, the conventional ischemic preconditioning protocol is both invasive and impractical to apply. The aim of the present study was to evaluate whether preconditioning with +Gz centrifuge acceleration (head-to-foot inertial load) which could induce brief episodes of sublethal ischemia in brain had neuroprotection against focal cerebral ischemic injury. A total of 85 male Sprague-Dawley rats were randomly assigned to five groups (n = 17 in each). The 2 Gz, 4 Gz, 6 Gz and 8 Gz groups were subjected to 3 min exposures at +2 Gz, +4 Gz, +6 Gz and +8 Gz, respectively for consecutive three times in animal centrifuge, with a 30-min rest period between each centrifuge run. The control group had no exposure to +Gz acceleration. Twenty-four hours after the last pretreatment, 12 rats in each groups were subjected to focal cerebral ischemia for 120 min and the other five rats in each group were sacrificed to measure the expression of heat shock protein 70(HSP70) in hippocampus by Western blot analysis. The results indicated that the 6 Gz and 8 Gz groups showed smaller infarct volume and lower neurologic deficit scores than the control group. The expression of HSP70 was significantly increased in 6 Gz and 8 Gz groups than those in the control group. Therefore, preconditioning with +Gz acceleration produced delayed neuroprotection against focal cerebral ischemia and that the neuroprotection may be related to the induction of HSP70.
机译:缺血预处理被认为是最强大的内源性神经保护剂。然而,常规的缺血预处理方案既有创性又不实用。本研究的目的是评估采用+ Gz离心机加速(头至脚惯性负载)进行预处理可能会导致脑中短暂致死性缺血的短暂发作,从而对局灶性脑缺血损伤具有神经保护作用。总共将85只Sprague-Dawley雄性大鼠随机分为5组(每组17只)。在动物离心机中,分别将2 Gz,4 Gz,6 Gz和8 Gz组分别在+2 Gz,+ 4 Gz,+ 6 Gz和+8 Gz下暴露3分钟,连续30次。每次离心机运行之间的休息时间。对照组没有暴露于+ Gz加速。最后一次预处理后24小时,每组12只大鼠进行局灶性脑缺血120分钟,并处死每组另5只大鼠,通过Western blot测定海马中热休克蛋白70(HSP70)的表达。分析。结果表明,与对照组相比,6 Gz和8 Gz组的梗死体积更小,神经功能缺损得分更低。 6 Gz和8 Gz组的HSP70表达明显高于对照组。因此,以+ Gz加速进行预处理会导致针对局灶性脑缺血的神经保护作用延迟,并且该神经保护作用可能与HSP70的诱导有关。

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