Neuroprotective effects of Scallop-derived plasmalogen in a mouse model of ischemic stroke
Neuroprotective effects of Scallop-derived plasmalogen in a mouse model of ischemic stroke
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扇贝缩醛磷脂对缺血性中风小鼠模型的神经保护作用
DOI：
10.1016/j.brainres.2021.147516
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发表时间：
2021
期刊：
影响因子：
2.9
通讯作者：
Abe Koji
中科院分区：
文献类型：
--
作者：
Feng Tian;Hu Xinran;Fukui Yusuke;Tadokoro Koh;Bian Zhihong;Morihara Ryuta;Yamashita Toru;Abe Koji
扇贝源性缩醛磷脂（sPlas）具有抗氧化和抗炎活性，但其功效尚未在缺血性中风模型中研究，其中氧化应激、炎症和神经血管单位（NVU）损伤加速病理生理学进展。因此，在本研究中，我们的目的是通过使用短暂性大脑中动脉闭塞（tMCAO）小鼠模型来评估sPlas在缺血性中风中的神经保护作用。在媒介物或sPlas（10 mg/kg/天）预处理14天后，成年雄性小鼠经受tMCAO 60分钟，然后在再灌注期间用媒介物或sPlas连续处理并再处理5天。施用sPlas显著改善了运动缺陷，（角落和旋转棒测试，*p< 0.05，相对于载体），增强血清抗氧化活性（OXY-吸附剂和d-ROM测试，*p< 0.05，相对于媒介物），梗死体积减少（*p< 0.05相对于媒介物），降低了两种氧化应激标志物4-HNE的表达，（*p< 0.05，相对于媒介物）和8-OHdG（*p< 0.05，相对于载体），降低促炎标志物Iba-1的表达01相对于媒介物）、IL-1β（**p< 0.01相对于媒介物）和TNF-α（**p<0.01相对于媒介物），并减轻NVU损伤（胶原IV、MMP 9和GFAP/胶原IV，*p< 0.05相对于媒介物）。我们的研究结果首次证实了sPlas通过抗氧化应激、抗炎和改善NVU损伤对tMCAO后5 d的急性缺血性卒中小鼠的神经保护作用，表明sPlas在预防和治疗缺血性卒中中的潜力。
Scallop-derived plasmalogen (sPlas) has both anti-oxidative and anti-inflammation activities, but its efficacy has not been investigated in ischemic stroke models where oxidative stress, inflammation, and neurovascular unit (NVU) damage accelerates pathophysiological progression. Therefore, in the present study, we aimed to assess the neuroprotective effects of sPlas in ischemic stroke by using a transient middle cerebral artery occlusion (tMCAO) mouse model. After the pretreatment of vehicle or sPlas (10 mg/kg/day) for 14 days, adult male mice were subjected to tMCAO for 60 min, then continuously treated with vehicle or sPlas during reperfusion and for an additional 5 days. The administration of sPlas significantly improved motor deficits (corner and rotarod tests, *p< 0.05 vs vehicle), enhanced serum antioxidative activity (OXY-adsorbent and d-ROMs tests, *p< 0.05 vs vehicle), reduced infarction volume (*p< 0.05 vs vehicle), decreased the expression of two oxidative stress markers, 4-HNE (*p< 0.05 vs vehicle) and 8-OHdG (*p< 0.05 vs vehicle), decreased the expression of pro-inflammatory markers Iba-1 (**p< 0.01 vs vehicle), IL-1β (**p< 0.01 vs vehicle), and TNF-α (**p< 0.01 vs vehicle), and alleviated NVU damage (collagen IV, MMP9, and GFAP/collagen IV, *p< 0.05 vs vehicle). Our present findings are the first to demonstrate the neuroprotective effects of sPlas on acute ischemic stroke mice at 5 d after tMCAO via anti-oxidative stress, anti-inflammation, and improvement of NVU damage, suggesting the potential of sPlas in preventing and treating ischemic stroke.