神经炎症
医学
冲程(发动机)
炎症
前蛋白转化酶
药理学
麻醉
内科学
低密度脂蛋白受体
机械工程
工程类
胆固醇
脂蛋白
作者
Yaling Zheng,Tianrui Zhu,Gang Li,Luran Xu,Y. Zhang
标识
DOI:10.1016/j.intimp.2023.111195
摘要
Ischemic stroke is the second leading cause of death worldwide, and neuroinflammation has been recognized as a critical player in its progression. Meanwhile, proprotein convertase subtilisin/kexin type 9 inhibitor (PCSK9i) has been demonstrated to inhibit inflammatory response. However, the effects of PCSK9i on ischemic stroke remain unclear and require further investigation. Temporary middle cerebral artery occlusion (tMCAO) was performed to establish animal models of ischemic stroke in C57BL/6 mice. The PCSK9i were administered subcutaneously after 2 h tMCAO. Neurological function and cerebral infarct volume were measured by mNSS and TTC staining, respectively. RNA-seq was performed to investigate the changes in mechanistic pathways. Western blotting and immunofluorescence were applied to detect expression of GPNMB, CD44, IL-6, and iNOS. Treatment with PCSK9i significantly improved neurological deficits and reduced the volume of cerebral infarction. PCSK9i suppressed neuroinflammation by activating the GPNMB/CD44 signaling pathway, further exerting their protective effects. Taken together, treatment with PCSK9i is an effective way to prevent ischemic stroke-induced brain injury.
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