Objective To explore the possible effect and mechanism of quercetin (QU) in inhibiting scar formation after the alkali burn of rat's cornea. Methods We established corneal alkali-burn model on right eyes of the SD rats. The rats were divided into five groups randomly. The control group received blank ophthalmic gel; the QU treatment groups received 2.5, 5, 10, or 20g/kg quercetin ophthalmic gel, respectively. The rats were checked by slit-lamp microscope every day for the degree of corneal opacity, then were killed on day 4, 7, 14, 21 and 28 after operation. The infiltration of the inflammatory cells was observed by histology, the arrangement and proliferation of the collagen fibers in the corneal stroma were observed by Masson trichrome staining. The expression of transforming growth factor-β_1 (TGF-β_1) and receptor of transforming growth factor-βⅠ(TGF-βRⅠ) in cornea was observed by immunohistochemical method. Results The corneal opacity was less severe in the QU treatment groups than in the control group (P<0.05). Corneal scar was inhibited better in 10g/kg QU and 20g/kg QU groups than in 2.5g/kg and 5g/kg QU groups, and 10g/kg and 20g/kg QU groups had no significant differences (P>0.05). HE and Masson staining showed that the density of corneal stroma collagen fibers in the QU treatment groups was lower than that in the control group. The expression of TGF-β_1 and TGF-βRⅠ reached the peak on day 7 after alkali burn, and then decreased slowly, which was close to the normal level. The expression of TGF-β_1 and TGF-βRⅠ was inhibited better in 10g/kg and 20g/kg QU groups than in 2.5g/kg and 5g/kg groups, and 10g/kg and 20g/kg QU groups had no significant differences (P>0.05). Conclusion QU ophthalmic gel can reduce formation of corneal scar to a certain extent, 10g/kg is the optimal concentration. QU may play its role by inhibiting the expression of TGF-β1 and TGF-βRⅠ.