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首页> 外文期刊>CNS neuroscience & therapeutics. >Kir6.1 Knockdown Aggravates Cerebral Ischemia/Reperfusion‐Induced Neural Injury in Mice
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Kir6.1 Knockdown Aggravates Cerebral Ischemia/Reperfusion‐Induced Neural Injury in Mice

机译：Kir6.1抑制基因加重小鼠的脑缺血/再灌注诱导的神经损伤

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Summary Background and Purpose ATP ‐sensitive potassium (K‐ ATP ) channels couple energy metabolism with electric activity, which play important roles in brain diseases including stroke. However, the impacts of Kir6.1‐containing K‐ ATP channels that mainly expressed on glia in stroke remain unclear. Methods and Results In this study, we found that expression of Kir6.1 was significantly decreased in the ischemic brain area of C57 BL /6J mice after 1‐h middle cerebral artery occlusion ( MCAO ) and 24‐h reperfusion. Then, we subjected Kir6.1 heterozygote knockout (Kir6.1+/?) mice to cerebral ischemia/reperfusion (I/R) injury and found that Kir6.1+/? mice exhibited exacerbated neurological disorder and enlarged infarct size, companied by glial over‐activation and blood–brain barrier ( BBB ) damages. Furthermore, we showed that Kir6.1 knockdown aggravated endoplasmic reticulum ( ER ) stress and thereby increased the levels of proinflammatory factors tumor necrosis factor‐α and interleukin‐1β ( TNF ‐α and IL ‐1β) in mouse brain. Conclusions Our findings reveal that Kir6.1 knockdown exacerbates cerebral I/R‐induced brain damages via increasing ER stress and inflammatory response, indicating that Kir6.1‐containing K‐ ATP channels may be a potential therapeutic target for stroke.
机译：小结背景和目的ATP敏感性钾（K- ATP）通道将能量代谢与电活动耦合，这在包括中风在内的脑部疾病中起着重要作用。但是，尚不清楚主要在中风的神经胶质中表达的含Kir6.1的K-ATP通道的影响。方法和结果在这项研究中，我们发现在1小时脑中动脉闭塞（MCAO）和24小时再灌注后，C57 BL / 6J小鼠的缺血性脑区域Kir6.1的表达显着降低。然后，我们对Kir6.1杂合子敲除（Kir6.1 + /？）小鼠进行了脑缺血/再灌注（I / R）损伤，结果发现Kir6.1 + /？小鼠表现出加剧的神经系统疾病和梗塞面积增大，伴有神经胶质过度活化和血脑屏障（BBB）损伤。此外，我们发现，Kir6.1基因敲低加重了内质网（ER）的应激，从而增加了小鼠脑中促炎因子，肿瘤坏死因子α和白介素1β（TNFα和IL-1β）的水平。结论我们的发现表明，通过增加ER应激和炎症反应，Kir6.1的敲低加剧了脑I / R诱导的脑损伤，表明含有Kir6.1的K- ATP通道可能是中风的潜在治疗靶点。

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