〔Abstract〕 Objective To investigate the role of mitochondrial fission and mitophagy in the model of bronchial epithelial cell injury induced by cigarette smoke extract. Methods Bronchial epithelial cells were co-cultured with 5% CSE,pretreated with mitochondrial fission inhibitor Mdivi-1(Md) and mitophagy inducer Urolithin A(UA).Cell proliferation, oxidative stress, mitochondrial structure, the mRNA levels of inflammatory factor(IL-1,IL-6,IL-18,CXCL 1,CXCL 8) and necroptosis components(RIPK1,RIPK3,MLKL),mitochondrial fission protein(DRP1,MFF) and mitophagy protein(p62/SQSTM1,LC3 B)were examined. Results In Beas 2 b cells, 5% CSE induced oxidative stress, increased the mRNA expression of inflammatory factor and necroptosis components, induced the destruction in mitochondrial network, increased the protein expression of mitochondrial fission and mitophagy protein p62/SQSTM1 expression and decreased mitophagy protein LC3 BⅡ/Ⅰ expression.Md/UA pretreatment inhibited oxidative stress, inhibited the expression of inflammatory factor mRNA and necroptosis components mRNA,partially restored mitochondrial network structure and decreased mitochondrial fission protein level.Md pretreatment increased mitophagy protein p62/SQSTM1 protein level, but did not affect LC3 BⅡ/Ⅰ protein expression.Pretreatment with UA inhibited p62/SQSTM1 protein expression, and increased LC3 BⅡ/Ⅰ protein expression. Conclusion Inhibiting mitochondrial fission or promoting mitophagy can reduce CSE-induced oxidative stress and inflammatory response, and restore mitochondrial structure.The mechanism may be related to the inhibition of mitochondrion fission and the mRNA expression of necroptosis components.