A new method for restoring damaged brain nerve function after stroke has been announced. The possibility of treatment by controlling the brain's inflammatory response has been suggested.

Professor Kim Byung-gon's research team (Research Instructor Kim Hyung-soon, Department of Brain Science, Ajou University College of Medicine) announced on the 20th that they had identified a new role of 'arginase enzyme protein', which maintains the balance of inflammatory response, in brain function recovery after stroke.

In our body, the inflammatory response plays a healing role in which a scab forms on a wounded skin, and the scab falls off and new flesh grows. However, this inflammatory response has a dual nature, causing pain when it is excessive and leading to delayed recovery due to chronic tissue ulcers.

'Arginase-1 enzyme protein' has been known as a beneficial substance that plays a balancing role in suppressing such excessive inflammatory response in tissues such as skin and liver and promoting tissue recovery, thereby maintaining a good balance between the contradictory aspects of the inflammatory response.

In this study using an ischemic stroke model, the research team observed that macrophages that induce inflammation infiltrate into brain tissue damaged by stroke, and the expression of arginase-1 protein increases a lot in these infiltrating macrophages.

It was confirmed that motor function was recovered when the excessive expression of arginase-1 protein was suppressed. In other words, it was confirmed that excessive expression of arginase-1 protein, which is known to maintain the balance of inflammatory response function, negatively affects functional recovery after stroke.

In particular, histological analysis revealed that suppression of arginase-1 protein expression inhibited the fibrotic reaction that blocks axon regeneration in damaged brain tissue and promoted the myelin formation reaction, which is important for nerve signal transmission in the lesion area.

Professor Kim Byung-gon said, "It is meaningful that we have for the first time demonstrated through an animal model that arginase-1, which was known as an anti-inflammatory phenotypic protein in conventional in vitro experiments, can play a negative role in functional recovery and inflammatory response after stroke."

He added, "We have presented a new target for developing a stroke treatment method using the oral arginase inhibitor OATD-02 (anti-cancer drug), which is currently undergoing clinical trials, and suggested the possibility of developing clinical translational research in the future."

Meanwhile, this research was published in February in the Proceedings of the National Academy of Sciences of the United States of America under the title 'Detrimental Influence of Arginase-1 in Infiltrating Macrophages on Post-Stroke Functional Recovery and Inflammatory Milieu'.

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