Acetylcorynoline inhibits microglia activation by regulating EGFR/MAPK signaling to promote functional recovery of injured mouse spinal cord

Spinal cord injury (SCI) is a serious neurological disease with a high disability rate that greatly reduces the quality of life for patients. Reducing secondary pathological damage, such as local inflammation in the injured spinal cord, through drug intervention is the main treatment. However, only methylprednisolone is currently approved by the FDA. This study explores the effects and mechanisms of acetylcorynoline (Ace) on functional recovery after spinal cord injury (SCI) in rats. The study found that Ace may promote tissue repair and motor function recovery after spinal cord injury by inhibiting microglia-mediated inflammatory responses by regulating the EGFR/MAPK pathway. The study used network pharmacology and molecular docking techniques to analyze the effects and possible molecular mechanisms of Ace in treating SCI. It observed the effect of Ace on microglia activation after SCI to provide a reference for clinical drug treatment.

• 1
  Ace treatment significantly increased the BBB score, reduced the area of spinal cord injury, and lowered the number of activated microglia cells and the levels of pro-inflammatory cytokines.
• 2
  Ace treatment significantly lower the level of cell activation and the production of inflammatory cytokines in LPS-treated BV2 cells.
• 3
  Network pharmacology analysis suggested that EGFR was the main target of Ace, and they bound to each other via hydrogen bonds as shown by molecular docking.