Background　It　is　well　established　that　airway　remodeling　and　inflammation　are　characteristics　for　chronic　obstructive　pulmonary　disease　(COPD).　Moreover,　cigarette　smoke　extract　(CSE)　promots　inflammation,　apoptosis　and　oxidative　stress　in　COPD.　And,　there　is　evidence　suggested　that　alantolactone　(ALT),　a　sesquiterpene　lactone　isolated　from　Inula　helenium,　plays　an　adverse　role　in　inflammation,　apoptosis　and　oxidative　stress.　However,　few　studies　have　investigated　the　function　and　mechanism　of　ALT　treatment　on　the　COPD　pathological　process.　Methods　The　levels　of　IL-1　beta,　TNF-alpha,　IL-6　and　IFN-gamma　were　examined　by　ELISA.　Cells＇　apoptosis　and　caspase-3　activity　were　detected　by　Cell　Death　Detection　PLUS　enzyme-linked　immunosorbent　assay　and　caspase-Glo　3/7　Assay,　respectively.　The　content　of　malondialdehyde　(MDA)　and　superoxide　dismutase　(SOD)　were　determined　by　using　MDA　and　SOD　assay　kits.　Reactive　oxygen　species　(ROS)　generation　was　measured　by　DCFH-DA　assay.　Protein　expression　was　assayed　by　Western　blot.　Results　In　the　present　study,　we　aimed　to　observe　the　protective　effects　of　ALT　against　inflammation,　apoptosis　and　oxidative　stress　in　human　bronchial　epithelial　Beas-2B　and　NHBE　cells.　Our　results　showed　that　different　doses　of　CSE　exposure　induced　Beas-2B　and　NHBE　cell　inflammatory　cytokines　IL-1　beta,　TNF-alpha,　IL-6　and　IFN-gamma　expression,　cell　apoptosis,　caspase-3　activity　and　mediated　oxidative　stress　markers　MDA,　ROS　and　SOD　levels,　while　ALT　treatment　counteracted　the　effects　of　CSE.　Further　studies　suggested　that　ALT　attenuated　NF-kappa　B　pathway　activation.　ALT　also　activated　the　Nrf2/HO-1　signal　pathway　through　promoting　Nrf2　nuclear　aggregation　and　downstream　HO-1　protein　expression.　HO-1　inhibitor　tin　protoporphyrin　IX　(SnPP　IX)　reversed　the　effects　of　ALT　on　Beas-2B　and　NHBE　cell　inflammation,　apoptosis　and　oxidative　stress.　Conclusions　The　above　results　collectively　suggested　that　ALT　suppressed　CSE-induced　inflammation,　apoptosis　and　oxidative　stress　by　modulating　the　NF-&　x138;B　and　Nrf2/　HO-1　axis.