Effects of imperatorin derivatives on the activity and drug resistance protein of alveolar type Ⅱ epithelial cells in COPD
- VernacularTitle:欧前胡素衍生物对COPD肺泡Ⅱ型细胞活性及耐药蛋白的影响
- Author:
Zhihong YU
1
;
Xiaoqin WANG
Author Information
- Keywords: pulmonary disease,chronic obstructive; imperatorin derivatives; alveolar type Ⅱ epithelial cells; cigarette smoke extract; multidrug resistance gene 1; multidrug resistance associated protein 1
- From: Tianjin Medical Journal 2024;52(11):1127-1131
- CountryChina
- Language:Chinese
- Abstract: Objective To explore effects of a derivative of imperatorin(IMP-1)on the activity and resistance proteins of alveolar type Ⅱ(ATⅡ)cells in chronic obstructive pulmonary disease(COPD).Methods AT Ⅱ cells were divided into the blank group(well growing AT Ⅱ cells cultured in conventional medium),the cigarette smoke extract(CSE)group(induced culture with 2%CSE added)and the IMP-1 group(intervention with 10 μ mol/L of IMP-1 on CSE induced AT Ⅱcells).Proliferation rates of AT Ⅱ cells at 24,48 and 72 hours were measured using MTT method.Apoptosis of ATⅡ cells was detected by Hoechst 33342 staining.The proportion of cells in each cycle was analyzed by flow cytometry.The number of ATⅡ cell clones was detected by soft AGAR clone formation assay.Multidrug resistance gene 1(MDR1)and multidrug resistance associated protein 1(MRP1)were detected by Western blot assay.Results Compared with the blank group,the apoptosis rate and the proportion of G0/G1 phase of ATⅡ cell cycle were increased in the CSE group,and the proliferation rate and the proportion of S,G2/M phase were decreased at 24 h,48 h and 72 h(P＜0.05).Compared with the CSE group,the cell proliferation rate,the proportion of S and G2/M phases and the number of cell clones were increased in the IMP-1 group,and the proportion of G0/G1 phase in ATⅡ cell cycle and the protein levels of MDR1 and MRP1 were decreased in the IMP-1 group(P＜0.05).Conclusion IMP-1 may downregulate the expression of MDR1 and MRP1 proteins induced by CSE in AT Ⅱ cells,inhibiting the progression of AT Ⅱ cells from S phase to G2 phase and from G2 phase to M phase,thereby inhibiting abnormal cell activation and increasing apoptosis.
