Abstract: Objective: To investigate the effect of allicin(ALL) on lung tissue damage and endoplasmic reticulum stress(ERS) in rats with chronic obstructive pulmonary disease(COPD). Methods: Sixty healthy adult male SD rats were randomly divided into normal control(NC) group, model group, allicin low(ALL-L, 4 mg/kg), allicin medium(ALL-M, 8 mg/kg), allicin high(ALL-H, 16 mg/kg) dose groups and dexamethasone(DXM, 1 mg/kg) group, with 10 rats in each group. The COPD rat models were established by repeated smoke exposure and intratracheal injection of lipopolysaccharide(except the rats in NC group). The drugs were given by intraperitoneal injection(the rats in NC group and model group were given physiological saline), once a day for 28 d. The pulmonary function indexes minute ventilation(MV), peak expiratory flow rate(PEF), forced vital capacity(FVC), forced expiratory volume in third second(FEV₃) and FEV₃/FVC were measured in each group, the histopathology changes of lung tissue was observed by HE staining and the apoptosis was observed by TUNEL staining; the contents of IL-1β, IL-6, TNF-α, and IFN-γ in alveolar lavage fluid were detected by ELISA; the expression of ERS related proteins was detected by western blotting. Results: Compared with the model group, the MV, PEF, FVC, FEV₃, and FEV₃/FVC in the ALL-M, ALL-H groups and DXM group were increased(P<0.05); the lung tissue pathological changes and apoptosis were significant improved, and the apoptosis index(AI) was decreased (P<0.05); the contents of IL-1β, IL-6, TNF-α, IFN-γwere decreased(P<0.05); the relative expression of GRP78, p-PERK, CHOP, NF-κB, Cleaved Caspase-12, Cleaved Caspase-3 were decreased(P<0.05). Except FEV₃/FVC, TNF-α and NF-κB, ALL-L, ALL-M and ALL-H groups showed dose-dependent effects on other indexes(P<0.05). Conclusion: ALL can reduce lung tissue damage and improve lung function in COPD rats and the mechanism may be related to inhibiting ERS and its mediated inflammatory response and apoptosis.