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Melatonin reduced volume of cerebral infarct induced by photothrombosis in wild-type mice, not in Cyclooxygenase-1 gene knockout mice

机译:褪黑激素减少野生型小鼠中由光致血栓形成引起的脑梗塞体积,而不是环氧合酶-1基因敲除小鼠

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摘要

Cyclooxygenase (COX) is crucial in inflammation and plays important role in cerebral ischemia. Anti-inflammatory effects of melatonin have been verified in previous studies. In this study, cerebral blood flow (CBF) was monitored during operation, infarct volume (IFV) was determined with 5-triphenyltetrazolium chloride (TTC) staining and MR image, and neurological functions were evaluated with turn in an alley and fall pole test in both COX-1-gene knockout and wide-type mice with or without melatonin administration 3 days after photothrombosis. CBF reduction, IFV and neurological deficits were not significantly different in COX-1 wild-type and COX-1 knockout mice. Melatonin (15 mg/kg) intraperitoneal injection decreased the CBF reduction, IFV and the latency to turn in an alley in COX-1 wide-type mice, whereas the neuroprotective effect of melatonin was attenuated in COX-1 knockout mice. We concluded that melatonin reduced susceptibility to photothrombotic stroke. COX-1 gene knockout does not alter the susceptibility to cerebral ischemia caused by photothrombosis. COX-1 plays an important role in the pathway of the protection of melatonin.
机译:环氧合酶(COX)在炎症中至关重要,并在脑缺血中起重要作用。褪黑激素的抗炎作用已在先前的研究中得到证实。在这项研究中,在手术过程中监测了脑血流量(CBF),用5-三苯基四唑氯化物(TTC)染色和MR图像确定了梗塞体积(IFV),并在胡同中通过转弯和落杆试验评估了神经功能。血栓形成后3天,无论是否服用褪黑素,都需要COX-1基因敲除小鼠和宽型小鼠。在COX-1野生型和COX-1基因敲除小鼠中,CBF降低,IFV和神经功能缺损没有显着差异。腹膜内注射褪黑激素(15 mg / kg)可降低COX-1宽型小鼠的CBF降低,IFV和转弯的潜伏期,而褪黑激素的神经保护作用在COX-1敲除小鼠中减弱。我们得出的结论是褪黑激素降低了对血栓形成性中风的敏感性。 COX-1基因敲除不会改变由光血栓形成引起的对脑缺血的敏感性。 COX-1在褪黑激素的保护途径中起着重要作用。

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