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环氧化酶-2介导高压氧预处理诱导的手术性脑损伤小鼠模型中的神经保护作用。

Cyclo-oxygenase-2 mediates hyperbaric oxygen preconditioning-induced neuroprotection in the mouse model of surgical brain injury.

作者信息

Jadhav Vikram, Ostrowski Robert P, Tong Wenni, Matus Brenden, Jesunathadas Rachel, Zhang John H

出版信息

Stroke. 2009 Sep;40(9):3139-42. doi: 10.1161/STROKEAHA.109.549774. Epub 2009 Jul 23.

DOI:10.1161/STROKEAHA.109.549774
PMID:19628811
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2798800/
Abstract

BACKGROUND AND PURPOSE

We investigated the role of cyclo-oxygenase-2 (COX-2) in mechanisms of hyperbaric oxygen preconditioning (HBO-PC) in the mouse model of surgical brain injury (SBI).

METHODS

C57BL mice were administered 100% oxygen for 1 hour at 2.5 atmosphere absolute for 5 consecutive days and subjected to SBI. Neurological status and brain edema were evaluated at 24 hours and 72 hours after the brain insult. Fluorescent immunostaining and Western blotting were performed to study hypoxia-inducible factor-1alpha and COX-2, respectively. Two doses of COX-2 inhibitor, NS398 (3 mg/kg and 10 mg/kg) were used to verify the role of COX-2 signaling pathway in the mechanism of HBO-PC.

RESULTS

HBO-PC improved neurological status and decreased brain edema at 24 hours and 72 hours after SBI. HBO-PC by itself and SBI independently increased COX-2 levels by 2-fold and 4-fold, respectively. HBO-PC, however, reduced increase in hypoxia-inducible factor-1alpha and COX-2 expression after SBI. The HBO-PC-induced improvement in neurological status and brain edema was reversed by a suboptimal dose of the COX-2 inhibitor, NS398 (10 mg/kg intraperitoneally; 1/4th of dose shown to provide neuroprotection), which itself had no effect on investigated end points.

CONCLUSIONS

HBO-PC attenuates postoperative brain edema and improves neurological outcomes after SBI. The HBO-PC-induced neuroprotection is mediated through COX-2 signaling pathways.

摘要

背景与目的

我们在手术性脑损伤（SBI）小鼠模型中研究了环氧化酶-2（COX-2）在高压氧预处理（HBO-PC）机制中的作用。

方法

将C57BL小鼠在2.5个绝对大气压下给予100%氧气1小时，连续5天，然后进行SBI。在脑损伤后24小时和72小时评估神经功能状态和脑水肿情况。分别进行荧光免疫染色和蛋白质印迹法来研究缺氧诱导因子-1α和COX-2。使用两剂COX-2抑制剂NS398（3毫克/千克和10毫克/千克）来验证COX-2信号通路在HBO-PC机制中的作用。

结果

HBO-PC改善了SBI后24小时和72小时的神经功能状态并减轻了脑水肿。HBO-PC本身和SBI分别使COX-2水平独立升高2倍和4倍。然而，HBO-PC降低了SBI后缺氧诱导因子-1α和COX-2表达的增加。COX-2抑制剂NS398的次优剂量（腹腔注射10毫克/千克；显示提供神经保护作用剂量的1/4）逆转了HBO-PC诱导的神经功能状态改善和脑水肿减轻，而该剂量本身对所研究的终点无影响。

结论

HBO-PC减轻了SBI后的术后脑水肿并改善了神经功能结局。HBO-PC诱导的神经保护作用是通过COX-2信号通路介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cec1/2798800/6c5bcaa040e2/nihms-139840-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cec1/2798800/245b49979e4e/nihms-139840-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cec1/2798800/95ddcc539a8e/nihms-139840-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cec1/2798800/6c5bcaa040e2/nihms-139840-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cec1/2798800/245b49979e4e/nihms-139840-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cec1/2798800/95ddcc539a8e/nihms-139840-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cec1/2798800/6c5bcaa040e2/nihms-139840-f0003.jpg

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