Abstract： Objective： To compare the therapeutic effects of different doses of Erzhi Pills on dry eye symptoms and inflammatory status induced by scopolamine in the mouse dry eye model， in order to explore the therapeutic effect and mechanism of Erzhi Pills in dry eyes. Methods：Thirty C57/BL6 mice were selected and divided into 5 groups，with 6 mice in each group. Among them，24 mice were induced into dry eye models by subcutaneous injection of scopolamine. They were ultimately divided into the blank control group (no dry eye model was established， oral administration of 1 mL of 0.9% sodium chloride solution)，the model group (after establishing a dry eye model，oral administration of 1 mL of 0.9% sodium chloride solution)，and the high-dose group (after establishing a dry eye model，oral administration of 12 g/kg of high-dose Erzhi Pills)，the medium-dose group (after establishing a dry eye model，oral administration of medium- dose Erzhi Pills 6 g/kg) and the low- dose group (after establishing a dry eye model， oral administration of low- dose Erzhi Pills 3 g/kg) were tested for changes in tear secretion and corneal fluorescein staining scores in each group on the first day before and the next day after modeling. The mice were euthanized 14 days later，and the corneal conjunctiva tissue was collected to detect the inflammatory factor tumor necrosis factor-α (TNF-α)，interleukin-1β (IL-1β)，IL-4 expression in the corneal conjunctiva tissue was detected using real- time quantitative PCR technology to detect changes in RNA levels. Flow cytometry was used to detect changes in protein levels using Cytometric Bead Array (CBA). Tear gland tissue was collected， and nuclear factors- κB (NF- κB) in the lacrimal gland were analyzed using Protein Simple's Wes fully automated protein blotting quantitative analysis system. Quantitative detection and validation of cytoplasmic and cytoplasmic validation were performed on pathway core protein P65 and phosphorylated P65. Results： After 14 days of medication， in terms of improving dry eye symptoms， compared with the model group，the tear secretion and corneal fluorescence staining scores of each dose group of Erzhi Pills were improved to varying degrees (P＜0.05). The treatment effect of the low-dose group and the medium dose-group was similar，while the treatment effect of the high-dose group was the best. In terms of improving ocular surface inflammation：①mRNA levels，compared with the model group，the mRNA levels of TNF- α， IL- 1β， IL- 4 in the high- dose group were significantly decreased， with statistically significant differences (P＜0.05). The mRNA expression levels of IL-4 in the high-，medium-， and low- dose groups were lower than those in the model group，with statistically significant differences (P＜0.05). It indicates that different doses of Erzhi Pills have inhibitory effects on the mRNA expression of ocular surface inflammatory factor IL- 4， but the high- dose group can also inhibit mRNA expression of TNF-α，IL-1β. ②Protein level：the protein expression levels of TNF-α， IL-1β in high-，medium-，and low-dose groups were lower than that of the model group，and the difference was statistically significant (P＜0.05). The protein expression of IL- 4 in each experimental group was lower than that in the model group，but the difference was not statistically significant (P＞0.05). Reminder of the effects of each dose of Erzhi Pills on the protein expression of TNF-α，IL-1β is inhibited，but the inhibitory effect on IL-4 protein expression was not significant. In terms of its impact on the lacrimal gland inflammation related pathways， Erzhi Pills in the high-，medium-，and low dose groups can inhibit the phosphorylation of intracellular P65 and the transport of phosphorylated P65 to the nucleus ， thereby inhibiting activation of the NF- κB pathway. Conclusion： Erzhi Pills can not only effectively improve tear secretion and corneal fluorescent pigment staining scores in dry eye mice，but also improve the inflammatory state of the ocular surface in dry eye mice. Its anti-inflammatory inhibitory effect on dry eye mice may be achieved by inhibiting NF- κB channel.