The　aim　of　this　study　was　to　investigate　the　effect　of　gallic　acid　(GA)　on　liver　fibrosis　induced　by　carbon　tetrachloride　(CCl4).　Male　BALB/c　mice　were　randomly　divided　into　four　groups:　normal　control　group　(group　A),　CCl4-induced　liver　injury　control　group　(group　B),　and　CCl4　induction　with　GA　of　low　dose　(5　mg/kg)　and　high　dose　(15　mg/kg)　treatment　group　(group　C　and　group　D).　GA　was　intra-gastric　given　for　mice　once　a　day　after　2　weeks　of　CCl4　induction.　Animals　were　killed　at　the　eighth　week.　Degrees　of　fibrosis　and　collagen　percentage　were　measured.　Hyaluronic　acid　(HA),　type　IV　collagen　(cIV),　malondialdehyde　(MDA),　alanine　aminotransferase　(ALT),　aspartate　aminotransferase　(AST),　and　gamma-glutamyl　transferase　(gamma-GT)　were　determined.　Expression　of　matrix　metalloproteinases-2　(MMP-2)　and　tissue　inhibitor　of　matrix　metalloproteinases-1　(TIMP-1)　mRNA　levels　were　examined　by　RT-PCR.　Western　blotting　was　carried　out　to　evaluate　the　changes　of　MMP-2　protein.　HE　and　VG　stainings　showed　GA　in　a　dose-dependent　manner　improved　significantly　the　fibrosis　condition　in　CCl4-injured　mice　(P　＜　0.05　or　P　＜　0.01).　Also,　the　concentrations　of　HA,　cIV,　and　MDA,　as　well　as　the　serum　levels　of　ALT,　AST,　and　gamma-GT　were　markedly　reduced　by　GA　(P　＜　0.05　or　P　＜　0.01),　and　decreases　in　MMP-2,　TIMP-1　mRNA,　and　MMP-2　protein　were　observed　as　well　(P　＜　0.05　or　P　＜　0.01).　GA　could　exert　protective　effect　on　liver　injury　and　reduce　liver　fibrosis　induced　by　CCl4　in　mice,　which　might　be　through　the　inhibition　of　hepatic　stellate　cell　activity.