Howell John Aaron, Gaouette Nicholas, Lopez Mariper, Burke Stephen P, Perkins Eddie, Bidwell Gene L
Graduate Program in Neuroscience, University of Mississippi Medical Center, Jackson, MS 39216.
Department of Neurology, University of Mississippi Medical Center, Jackson, MS 39216.
bioRxiv. 2023 Mar 15:2023.03.15.532834. doi: 10.1101/2023.03.15.532834.
Inflammatory processes are activated following ischemic strokes and lead to increased tissue damage for weeks following the ischemic insult, but there are no approved therapies that target this inflammation-induced secondary injury. Here, we report that SynB1-ELP-p50i, a novel protein inhibitor of the nuclear factor kappa B (NF-κB) inflammatory cascade bound to drug carrier elastin-like polypeptide (ELP), is able to enter both neurons and microglia, cross the blood-brain barrier, localize exclusively in the ischemic core and penumbra in Wistar-Kyoto and spontaneously hypertensive rats (SHRs), and reduce infarct volume in male SHRs. Additionally, in male SHRs, SynB1-ELP-p50i treatment improves survival for 14 days following stroke with no effects of toxicity or peripheral organ dysfunction. These results show high potential for ELP-delivered biologics for therapy of ischemic stroke and other central nervous system disorders and further support targeting inflammation in ischemic stroke.
缺血性中风后炎症过程被激活,并在缺血性损伤后的数周内导致组织损伤增加,但目前尚无针对这种炎症诱导的继发性损伤的获批疗法。在此,我们报告,SynB1-ELP-p50i是一种与药物载体弹性蛋白样多肽(ELP)结合的新型核因子κB(NF-κB)炎症级联反应蛋白抑制剂,它能够进入神经元和小胶质细胞,穿过血脑屏障,特异性地定位于Wistar-Kyoto大鼠和自发性高血压大鼠(SHR)的缺血核心区和半暗带,并减少雄性SHR的梗死体积。此外,在雄性SHR中,SynB1-ELP-p50i治疗可改善中风后14天的生存率,且无毒性或外周器官功能障碍的影响。这些结果表明,ELP递送的生物制剂在治疗缺血性中风和其他中枢神经系统疾病方面具有很高的潜力,并进一步支持针对缺血性中风中的炎症进行治疗。