Effects of RO27-3225 on neurogenesis, PDGFRβ+ cells and neuroinflammation after cerebral infarction

What the hell are your doctors and stroke hospital doing to ensure that human testing occurs? Waiting for SOMEONE ELSE TO SOLVE THE PROBLEM is pure incompetency.  I'd suggest having survivors run that stroke hospital. We finally would get stroke solved. Current stroke leaders have been failing for 50+ years, we can't do worse.

Effects of RO27-3225 on neurogenesis, PDGFRβ⁺ cells and neuroinflammation after cerebral infarction

Author links open overlay panelYongxinZhang^aJianpingWang^b

DiZhang^aZhengfangLu^aJiangMan^a

https://doi.org/10.1016/j.intimp.2020.106281Get rights and content

Highlights

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RO27-3225 promoted neurogenesis in the SVZ after tMCAO.

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RO27-3225 increased the number of PDGFRβ⁺ cells in the peri-infarct area after tMCAO.

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RO27-3225 inhibited neuroinflammation in the peri-infarction zone after tMCAO.

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RO27-3225 ameliorated brain damage and improved recovery of neurological function after tMCAO.

Abstract

Cerebral infarction causes severe social and economic burdens to patients due to its high morbidity and mortality rates, and the available treatments are limited. RO27-3225 is a highly selective melanocortin receptor 4 agonist that alleviates damage in many nervous system diseases, such as cerebral hemorrhage, traumatic brain injury and chronic neurodegenerative diseases. However, the effect of RO27-3225 on cerebral infarction remains unclear. In this study, we used a mouse model of transient middle cerebral artery occlusion (tMCAO) and administered RO27-3225 or saline to the mice through intraperitoneal injection. RO27-3225 increased the number of Nestin⁺/BrdU⁺ cells and doublecortin (DCX)⁺/BrdU⁺ cells in the subventricular zone (SVZ) and the number of DCX⁺/BrdU⁺ cells in the peri-infarct area on day 7 after tMCAO. Furthermore, RO27-3225 decreased the number of activated microglia (Iba1⁺ cells with a specific morphology) and the expression levels of Iba1, TNFα, IL6, and iNOS proteins and increased the number of PDGFRβ⁺ cells in the periinfarct region on day 3 after tMCAO. Finally, RO27-3225-treated mice exhibited significantly decreased infarct volumes, brain water contents, and neurological deficits after cerebral infarction. Thus, RO27-3225 can improve the outcomes following cerebral infarction, partially by regulating neurogenesis in the SVZ, PDGFRβ⁺ cell survival and neuroinflammation in the periinfarct zone. Our research reveals that RO27-3225 is a potential new treatment for cerebral infarction.