Alternatively, BBG significantly down-regulated hepatic TGF-β, p-ERK, and α-SMA protein expressions (CBDL-vehicle vs. CBDL-BBG: [/β-actin]: TGF-β: 0.8646±0.1516 vs. 0.4776±0.0530, p = 0.037; ERK: 0.6471±0.1477 vs. 0.6550±0.1225, p = 0.9673; α-SMA: 0.4568±0.0211 vs. 0.3805±0.0217, p = 0.027 [p-ERK/ERK]: 2.1460±0.2410 vs. 1.0765±0.2739, p = 0.015), suggesting that BBG improved CBDL-induced liver fibrosis via the non-Smad signaling pathway. Here, TGFB1 is linked to Hepatic fibrosis.