2. Academic Validation
  3. Evaluation of cigarette smoke-induced oxidative stress and inflammation in BEAS-2B cells based on a lung microfluidic chip

Evaluation of cigarette smoke-induced oxidative stress and inflammation in BEAS-2B cells based on a lung microfluidic chip

  • Food Chem Toxicol. 2023 Apr 14;176:113787. doi: 10.1016/j.fct.2023.113787.
Jingxian Xue 1,  Zezhi Li 2,  Xiang Li 3,  Chenfeng Hua 1,  Pingping Shang 1,  Junwei Zhao 1,  Kejian Liu 1,  Fuwei Xie 4
Affiliations

Affiliations

  • 1 Key Laboratory of Tobacco Chemistry, Zhengzhou Tobacco Research Institute of CNTC, No. 2 Fengyang Street, Zhengzhou, 450001, PR China.
  • 2 Key Laboratory of Tobacco Chemistry, Zhengzhou Tobacco Research Institute of CNTC, No. 2 Fengyang Street, Zhengzhou, 450001, PR China; Beijing Technology and Business University, Beijing, 100048, PR China.
  • 3 Key Laboratory of Tobacco Chemistry, Zhengzhou Tobacco Research Institute of CNTC, No. 2 Fengyang Street, Zhengzhou, 450001, PR China. Electronic address: [email protected].
  • 4 Key Laboratory of Tobacco Chemistry, Zhengzhou Tobacco Research Institute of CNTC, No. 2 Fengyang Street, Zhengzhou, 450001, PR China. Electronic address: [email protected].
PMID: 37062330 DOI: 10.1016/j.fct.2023.113787
Abstract

Oxidative stress and inflammation induced by cigarette smoking are associated with the pathology process of various chronic respiratory diseases, including asthma, emphysema, chronic obstructive pulmonary disease and Cancer. Compared with conventional Cell Culture techniques, microfluidic chips can provide a continuous nutrient supply, mimic the in vivo physiological microenvironment of the cells, and conduct an integrated and flexible analysis of cell status and functions. Here, we designed and fabricated a bionic-lung chip, which was applied to perform cigarette smoke exposure of BEAS-2B cells cultured at the gas-liquid interface. The oxidative stress and inflammation in the cells exposed to cigarette smoke were investigated on chip. The results showed that cellular damage, oxidative stress and inflammatory response induced by cigarette smoke in the chip were dependent on smoke concentration and time after smoke exposure. N-Acetylcysteine (NAC) significantly inhibited these effects of cigarette smoke exposure on the cells at the gas-liquid interface within the chip.

Keywords

Cigarette smoke; Gaseous pollutants; Inflammation; Microfluidic chip; Reactive oxygen species.

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