Inactivation of hepatic stellate cells (HSCs) slows down liver cirrhosis (LC) advancement. The role of circular RNAs (circRNAs) in LC is largely undiscovered. Here, we clarified the effect of circCHD2 on HSCs. LX-2 cells were stimulated with TGF-β1 to establish a cell model. The circCHD2, miR-200b-3p, and HLF were inspected using quantitative real-time PCR (qPCR). Cell counting kit-8, 5-Ethynyl-2'-deoxyuridine, together with colony formation assays were all conducted to analyze cell proliferation. α-SMA and Col1A1 were evaluated by qPCR and Western blot. The targets of circCHD2 and miR-200b-3p were verified by luciferase reporter assay. We found the circCHD2 was upregulated in the patients with LC and transforming growth factor beta 1 (TGF-β1)-stimulated LX-2 cells. Interfering of circCHD2 inhibited the proliferation induced by TGF-β1, downregulated α-SMA, and Col1A1. CircCHD2 served as a miR-200b-3p sponge, which directly targeted downstream HLF. Downregulated miR-200b-3p abrogated suppression on the cellular process, α-SMA and Col1A1 levels induced by knockdown of circCHD2. Enforced HLF reversed the effect induced by miR-200b-3p overexpression. Taken together, a loss of circCHD2/miR-200b-3p/HLF axis contributed to alleviate LC progression. The findings suggested that circCHD2 may have potential to be a therapeutic target of LC.