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首页> 外文期刊>The Canadian Journal of Neurological Sciences: le Journal Canadien des Sciences Neurologiques >Low-Intensity Ultrasound Decreases Ischemia-Induced Edema by Inhibiting N-Methyl-d-Aspartic Acid Receptors
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Low-Intensity Ultrasound Decreases Ischemia-Induced Edema by Inhibiting N-Methyl-d-Aspartic Acid Receptors

机译：低强度超声通过抑制N-甲基-D-天冬氨酸受体来降低缺血诱导的水肿

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Background: We have previously shown that low-intensity ultrasound (LIUS), a noninvasive mechanical stimulus, inhibits brain edema formation induced by oxygen and glucose deprivation (OGD) or treatment with glutamate, a mediator of OGD-induced edema, in acute rat hippocampal slice model in vitro. Methods: In this study, we treated the rat hippocampal slices with N-methyl-d-aspartic acid (NMDA) or (S)-3,5-dihydroxyphenylglycine (DHPG) to determine whether these different glutamate receptor agonists induce edema. The hippocampal slices were then either sonicated with LIUS or treated with N-methyl-d-aspartic acid receptor (NMDAR) antagonists, namely, MK-801 and ketamine, and observed their effects on edema formation. Results: We observed that treatment with NMDA, an agonist of ionotropic glutamate receptors, induced brain edema at similar degrees compared with that induced by OGD. However, treatment with DHPG, an agonist of metabotropic glutamate receptors, did not significantly induce brain edema. Treatment with the NMDAR antagonists MK-801 or ketamine efficiently prevented brain edema formation by both OGD and NMDA in a concentration-dependent manner. N-Methyl-d-aspartic acid-induced brain edema was alleviated by LIUS in an intensity-dependent manner when ultrasound was administered at 30, 50, or 100 mW/cm2 for 20 minutes before the induction of the edema. Furthermore, LIUS reduced OGD- and NMDA-induced phosphorylation of NMDARs at Y1325. Conclusion: These results suggest that LIUS can inhibit OGD- or NMDA-induced NMDAR activation by preventing NMDAR phosphorylation, thereby reducing a subsequent brain edema formation. The mechanisms by which LIUS inhibits NMDAR phosphorylation need further investigation.
机译：背景：我们之前已经表明，低强度超声（LiS），非侵袭性机械刺激，抑制氧气和葡萄糖剥夺（OGD）诱导的脑水肿或用谷氨酸处理，急性大鼠海马的介质诱导的水肿，抑制葡萄糖（OGD）或治疗。体外切片模型。方法：在本研究中，我们用N-甲基-D-天冬氨酸（NMDA）或（S）-3,5-二羟基苯基甘氨酸（DHPG）对大鼠海马切片进行了处理，以确定这些不同的谷氨酸受体激动剂是否诱导水肿。然后用Lius超声处理海马切片或用N-甲基-D-天冬氨酸受体（NMDAR）拮抗剂，即MK-801和氯胺酮处理，并观察到它们对水肿形成的影响。结果：我们观察到与NMDA的治疗，离子淋谷氨酸受体的激动剂，与OGD诱导的相比，在类似程度上诱导脑水肿。然而，用DHPG治疗，代谢谷氨酸受体的激动剂，没有显着诱导脑水肿。用NMDAR拮抗剂MK-801或氯胺酮的处理有效地通过OGD和NMDA以浓度依赖性方式形成脑水肿。当超声在水肿诱导前20分钟时，通过Lius通过强度依赖性方式减轻了N-甲基-D-天冬氨酸诱导的脑水肿。此外，Lius在Y1325下降低了OGD-和NMDA诱导的NMDARS的磷酸化。结论：这些结果表明LiS可以通过防止NMDAR磷酸化抑制OGD-或NMDA诱导的NMDAR活化，从而减少随后的脑水肿形成。 Lius抑制NMDAR磷酸化的机制需要进一步调查。

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