Apigenin inhibits fibrous scar formation after acute spinal cord injury through TGFβ/SMADs signaling pathway

Aim: To investigate the effect of apigenin on fibrous scar formation after mouse spinal cord injury (SCI). Methods: The pneumatic impactor strike method was used to establish an SCI model. Mice were intraperitoneally injected with 5 mg/kg or 20 mg/kg apigenin daily for 28 days after SCI. The Basso Mouse Scale (BMS) score, hematoxylin-eosin staining, and immunohistochemical staining were used to assess the effect of apigenin on scar formation and motor function recovery. Western blotting and qRT-PCR were used to detect the expression of fibrosis-related parameters in spinal cord tissue homogenates. NIH-3 T3 cells and mouse primary spinal cord fibroblasts, alpha-Smooth muscle actin (alpha-SMA), collagen 1, and fibronectin were used to evaluate apigenin's effect in vitro. Western blotting and immunofluorescence techniques were used to study the effect of apigenin on TGF beta/SMADs signaling. Results: Apigenin inhibited fibrous scar formation in the mouse spinal cord and promoted the recovery of motor function. It reduced the expression of fibroblast-related parameters and increased the content of nerve growth factor in vivo, decreasing myofibroblast activation and collagen fiber formation by inhibiting TGF beta-induced SMAD2/3 phosphorylation and nuclear translocation in vitro. Conclusion: Apigenin inhibits fibrous scar formation after SCI by decreasing fibrosis-related factor expression through TGF beta/SMADs signaling.

Automated summary

This study investigated the effect of apigenin on fibrous scar formation after spinal cord injury (SCI) in mice. Results showed that apigenin inhibited fibrous scar formation and promoted motor function recovery. It achieved this by reducing the expression of fibrosis-related factors through the TGF beta/SMADs signaling pathway.