FIGURE 8.

Schematic illustration of Pae attenuated vascular fibrosis through regulating Treg/Th17 balance in a gut microbiota-dependent manner. The gut microbiota of AS mice was disordered, causing the balance of Treg/Th17 cells to tilt toward Th17 cells, inducing the increase in LOX expression in the aorta, thereby promoting vascular fibrosis. Pae can increase the abundance of short-chain fatty acid-producing bacteria to directly upregulate SCFA levels in AS mice, leading to the decrease in LOX expression by restoring the Treg/Th17 balance, thereby inhibiting vascular fibrosis, which was an important mechanism of Pae in improving vascular fibrosis.