Among these the high binding energies of α-amyrin with TNF and tanshinone IIA with IL-6 indicate that these components can directly inhibit the activity of pro-inflammatory factors and block the abnormal activation of downstream signaling pathways such as IL-17 and sphingolipid metabolism, thereby regulating the LncRNA network associated with HSC activation and, ultimately, alleviating the progression of liver fibrosis. The gene discussed is IL17A; the disease is Hepatic fibrosis.