Among these, CDKN1A, NR1I3, and TUBB1, which can concurrently interact with quercetin, were associated with the prognosis of liver fibrosis, indicating that HXS may inhibit or reverse HSC activation primarily by suppressing neutrophil extracellular trap formation, stimulating oxidative phosphorylation and promoting thyroid hormone synthesis in the regulation of the liver microenvironment. This evidence concerns the gene NR1I3 and Hepatic fibrosis.