Objective：To investigate the relationship between acidic deoxycholic acid induced mitochondrial DNA（mtDNA） damage and release of human esophageal epithelial cells and cGAS -STING pathway in the development of esophageal epithelial cell inflammation. Methods：HEECs were divided into control group and acidic deoxycholic acid treatment group. The viability of cells was measured by CCK -8 assay. Changes of reactive oxygen species，mitochondrial reactive oxygen species and mitochondrial membrane potential were detected by fluorescence microscope and flow cytometry. ATP was detected by the luminometer. The ultrastructure of mitochondria was observed by transmission electron microscope. The mtDNA copy number was evaluated by qPCR. The expressions of γH2AX，cGAS，STING，p -NF -κB p65 and NF -κB p65 were detected by Western blotting. The mRNA expressions of inflammatory cytokines IL-6 and IL-1β were detected by qPCR. Results：CCK-8 assay showed that the viability of cells treated with acidic deoxycholic acid decreased in a dose-time dependent manner. The production of intracellular ROS and mtROS increased，while MMP and ATP decreased. Compared with the control group，the expression of γH2AX increased after acidic deoxycholic acid，mtDNA released into the cytoplasm，mtDNA copy number reduced，the expressions of cGAS，STING and p-NF-κB p65 were increased，and the expressions of inflammatory cytokines IL-6 and IL-1β were elevated. After pretreatment with cGAS inhibitor RU.521，the expression levels of cGAS and STING were inhibited and the expression of p-NF-κB p65 was partially inhibited，and the levels of inflammatory cytokines IL-6 and IL-1β were decreased. Conclusion：The in vitro experiments have shown that acidic deoxycholic acid can induce mitochondrial dysfunction，mitochondrial DNA damage and release，and mediate HEEC inflammation. The mechanism may be related to the activation of cGAS-STING pathway.