1.NF-κB inhibitor or NAC attenuates amiodarone-induced injury of human lung epithelial cell line BEAS-2B
Zezhao JI ; Qi ZHANG ; ABUDUXUKUER·ABULIMITI
Basic & Clinical Medicine 2025;45(8):1010-1015
Objective To investigate the mechanism of reactive oxygen species(ROS)and pyroptosis in amioda-rone-induced lung epithelial cell injury.Methods The viability of cells treated with amiodarone,amiodarone+N-acetylcysteine(ROS inhibitor,NAC)and amiodarone+NF-κB inhibitors was detected by MTT assay.ROS level was detected by DCFA probe and the levels of IL-6,IL-18,IL-1β and TNF-α in the supernatant were detected by ELISA;NLRP3.Caspase-1 p20 and GSDMD-N protein were detected by Western blot.Results Amiodarone con-centration-dependently reduced cell viability(P<0.05),NAC and NF-κB attenuated the cytotoxicity of amiodarone(P<0.05).Amiodarone increased levels of reactive oxygen species,inflammatory factors and pyroptosis-related proteins in lung epithelial cells(P<0.05),while NAC and NF-κB inhibitors reduced the levels of these indicators(P<0.05).Conclusions NF-κB inhibitor or NAC attenuates amiodarone-induced injury of human lung epithelial cell line in vitro.
2.NF-κB inhibitor or NAC attenuates amiodarone-induced injury of human lung epithelial cell line BEAS-2B
Zezhao JI ; Qi ZHANG ; ABUDUXUKUER·ABULIMITI
Basic & Clinical Medicine 2025;45(8):1010-1015
Objective To investigate the mechanism of reactive oxygen species(ROS)and pyroptosis in amioda-rone-induced lung epithelial cell injury.Methods The viability of cells treated with amiodarone,amiodarone+N-acetylcysteine(ROS inhibitor,NAC)and amiodarone+NF-κB inhibitors was detected by MTT assay.ROS level was detected by DCFA probe and the levels of IL-6,IL-18,IL-1β and TNF-α in the supernatant were detected by ELISA;NLRP3.Caspase-1 p20 and GSDMD-N protein were detected by Western blot.Results Amiodarone con-centration-dependently reduced cell viability(P<0.05),NAC and NF-κB attenuated the cytotoxicity of amiodarone(P<0.05).Amiodarone increased levels of reactive oxygen species,inflammatory factors and pyroptosis-related proteins in lung epithelial cells(P<0.05),while NAC and NF-κB inhibitors reduced the levels of these indicators(P<0.05).Conclusions NF-κB inhibitor or NAC attenuates amiodarone-induced injury of human lung epithelial cell line in vitro.
3.FER-1 inhibits methylglyoxal-induced ferroptosis in mouse alveolar macrophages in vitro.
Qi ZHANG ; Zezhao JI ; Abai JIASHAER ; Youda WANG ; ABUDUXUKUER ABULIMITI
Journal of Southern Medical University 2024;44(12):2443-2448
OBJECTIVES:
To investigate the inhibitory effect of FER-1 on methylglyoxal-induced ferroptosis in cultured mouse alveolar macrophages.
METHODS:
MH-S cells derived from mouse alveolar macrophages treated with 90 μg/mL methylglyoxal, 10 μmol/mL FER-1MG+FER-1, or both were examined for intracellular reactive oxygen species (ROS), malondialdehyde (MDA) and ferrous ion (Fe2+) levels and changes in mitochondrial membrane potential. Western blotting was performed to detect the protein expression levels of glutathione peroxidase 4 (GPX4) and long-chain acyl-CoA synthase 4 (ACSL4).
RESULTS:
Methylglyoxal treatment of MH-S cells for 24 h significantly decreased the protein expression level of GPX4, upregulated the protein expression of ACSL4, increased intracellular concentrations of ferrous ions, ROS and MDA, caused loss of mitochondrial membrane potential, and decreased cell viability. Treatment of the cells with FER-1 effectively attenuated these detrimental effects of methylglyoxal in MH-S cells by increasing GPX4 expression, reducing ACSL4 expression and intracellular ferrous ions, ROS and MDA levels, and restoring the mitochondrial membrane potential.
CONCLUSIONS
Methylglyoxal can induce ferroptosis in MH-S cells in a dose-dependent manner, and FER-1 can rescue the cells from methylglyoxal-induced ferroptosis.
Animals
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Ferroptosis/drug effects*
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Mice
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Pyruvaldehyde
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Macrophages, Alveolar/drug effects*
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Reactive Oxygen Species/metabolism*
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Phospholipid Hydroperoxide Glutathione Peroxidase/metabolism*
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Membrane Potential, Mitochondrial/drug effects*
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Coenzyme A Ligases/metabolism*
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Malondialdehyde/metabolism*
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Cell Survival/drug effects*
4.Numerical simulation of the multi-dimensional phase-change problem in cryosurgery.
Jiangang JI ; Jie ZHANG ; Zezhao HUA
Journal of Biomedical Engineering 2005;22(4):759-764
The phase change process in cryosurgery is simulated here with finite element scheme. The calculated results are consistent with experimental results. The compared results confirm the feasibility of the enthalpy model and finite element simulation method. And the successive Freeze-thawing Circle and multi-probe cryosurgery process are further simulated and the characteristic of the thermal field and thermal gradient around cryoprobe are analyzed. The application of enthalpy mathematical model and finite element scheme provide useful simulating means for the cryosurgery and will be beneficial for the progressing and extending of the cryosurgery technology.
Computer Simulation
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Cryosurgery
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methods
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Finite Element Analysis
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Humans
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Models, Theoretical
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Phase Transition

Result Analysis
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