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黑种草子对蛛网膜下腔出血大鼠模型氧化损伤的影响。

The effects of Nigella sativa against oxidative injury in a rat model of subarachnoid hemorrhage.

机构信息

Department of Neurosurgery, Haydarpasa Numune Education and Research Hospital, Istanbul, Turkey.

出版信息

Acta Neurochir (Wien). 2011 Feb;153(2):333-41. doi: 10.1007/s00701-010-0853-9. Epub 2010 Nov 12.

Abstract

OBJECTIVE

The aim of the study was to investigate the putative neuroprotective effect of Nigella sativa oil (NSO) treatment against subarachnoid hemorrhage (SAH) in rats.

METHODS

To induce SAH, rats were injected with 0.3 ml blood into their cisterna magna. Male Wistar albino rats were divided as control, vehicle-treated SAH, and NSO-treated (0.2 ml/kg, intraperitoneally) SAH groups. Forty-eight hours after SAH induction, neurological examination scores were recorded and the rats were decapitated. Brain tissue samples were taken for blood brain barrier permeability, brain water content, or determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO), and Na(+)-K(+)-ATPase activities.

RESULTS AND DISCUSSION

On the second day of SAH induction, neurological examination scores were increased in SAH groups, while SAH caused significant decreases in brain GSH content and Na(+)-K(+)-ATPase activity, which were accompanied with significant increases in MDA levels and MPO activity. The histological observation showed vasospasm of the basillary artery. On the other hand, NSO treatment markedly improved the neurological scores while all oxidant responses were prevented, implicating that NSO treatment may be of therapeutic use in preventing oxidative stress due to SAH.

摘要

目的

本研究旨在探讨黑种草籽油(Nigella sativa oil,NSO)治疗对大鼠蛛网膜下腔出血(subarachnoid hemorrhage,SAH)的潜在神经保护作用。

方法

为诱导 SAH,向大鼠脑池内注射 0.3ml 血液。雄性 Wistar 白化大鼠分为对照组、载药处理的 SAH 组和 NSO 处理(0.2ml/kg,腹腔内注射)的 SAH 组。在 SAH 诱导后 48 小时,记录神经学检查评分,然后断头处死大鼠。采集脑组织样本,用于测定血脑屏障通透性、脑水含量,或测定丙二醛(malondialdehyde,MDA)和谷胱甘肽(glutathione,GSH)水平、髓过氧化物酶(myeloperoxidase,MPO)和 Na(+)-K(+)-ATP 酶活性。

结果与讨论

在 SAH 诱导的第二天,SAH 组的神经学检查评分增加,而 SAH 导致大脑 GSH 含量和 Na(+)-K(+)-ATP 酶活性显著降低,同时 MDA 水平和 MPO 活性显著升高。组织学观察显示基底动脉血管痉挛。另一方面,NSO 治疗显著改善了神经学评分,同时所有的氧化应激反应都得到了预防,这表明 NSO 治疗可能对预防由于 SAH 引起的氧化应激具有治疗作用。

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