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Culturing of Human Nasal Epithelial Cells at the Air Liquid Interface
Published on: October 8, 2013
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Quercitrin protects human bronchial epithelial cells from oxidative damage.
Dan Yu1, Fan Wang2, Shuming Ye3
1Department of Hematology, Wuhan No. 1 Hospital, Wuhan 43022, Hubei, China.
Open Medicine (Warsaw, Poland)
|July 8, 2022
Summary
Quercitrin (QE) protects human bronchial epithelial cells (HBECs) from cigarette smoke extract (CSE)-induced damage. QE reduces apoptosis and oxidative stress by inhibiting the Nrf2/HO-1/NQO1 and MAPK/ERK pathways.
Area of Science:
- Pulmonary Medicine
- Cell Biology
- Toxicology
Background:
- Cigarette smoking (CS) is a primary cause of chronic obstructive pulmonary disease (COPD).
- Oxidative stress plays a crucial role in COPD pathogenesis.
- Cigarette smoke extract (CSE) induces apoptosis and oxidative stress in human bronchial epithelial cells (HBECs).
Purpose of the Study:
- To investigate the protective effects of quercitrin (QE) against CSE-induced apoptosis and oxidative stress in HBECs.
- To elucidate the underlying molecular mechanisms of QE's protective action.
Main Methods:
- Establishment of an in vitro COPD cellular model using HBECs treated with 2% CSE.
- Assessment of cell viability and apoptosis using CCK-8 assay and flow cytometry.
- Examination of protein levels via Western blotting and oxidant/antioxidant markers using ELISA kits.
Main Results:
- CSE significantly increased apoptosis and decreased viability in HBECs, effects reversed by QE.
- QE treatment restored oxidant/antioxidant balance, decreasing MDA and reactive oxygen species (ROS) while increasing T-AOC, SOD, and GSH peroxidase.
- QE reversed CSE-induced Nrf2 nuclear translocation and suppressed NQO1 and HO-1 expression, while also inhibiting MAPK/ERK signaling.
Conclusions:
- Quercitrin (QE) demonstrates significant protective effects against CSE-induced cell apoptosis and oxidative damage in HBECs.
- QE exerts its protective role by inactivating the Nrf2/HO-1/NQO1 and MAPK/ERK signaling pathways.
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