Salvianolic acid A improves nerve regeneration and repairs nerve defects in rats with brain injury by downregulating miR‐212‐3p‐mediated SOX7

Abstract

Abstract This study was to probe the protective effects and mechanisms of salvianolic acid A (SAA) on cerebral ischemia–reperfusion injury (CIRI). The middle cerebral artery occlusion model (MCAO) was established in rats. Rats' behavior, neurological deficits, brain injury, inflammation, and apoptosis in the brain tissue were evaluated. The inflammatory response and apoptosis of PC12 cells induced by oxygen glucose deprivation/reperfusion (OGD/R) were detected. SAA‐mediated changes in miR‐212‐3p, SOX7, and Wnt/β‐catenin pathway were determined, and the targeting relationship between miR‐212‐3p and SOX7 was clarified. SAA alleviated the neurological deficits and brain injury of MCAO rats and inhibited the inflammatory response and apoptosis of OGD/R‐conditioned PC‐12 cells. SAA upregulated miR‐212‐3p, Wnt3a, and β‐catenin, whereas inhibited SOX7 levels. Silencing miR‐212‐3p counteracted the protective effect of SAA in the context of CIRI. SOX7 was a target protein of miR‐212‐3p. Silencing SOX7 based on SAA and miR‐212‐3p knockdown suppressed OGD/R‐induced inflammation and apoptosis and increased Wnt3a and β‐catenin levels in PC12 cells. SAA can improve the brain and nervous system injury caused by cerebral ischemia–reperfusion by upregulating miR‐212‐3p, thereby inhibiting SOX7 and activating the Wnt/βcatenin signaling pathway.

Keywords

• cerebral ischemia–reperfusion injury
• miR‐212‐3p
• salvianolic acid A
• SOX7