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Bioinformatics Analysis and Experimental Validation of Epigallocatechin-3-gallate Against Iopromide-induced Injury in
Yuh-Feng Tsai1,2, Chia-Wen Tsai3,4,5, Jai-Sing Yang5
1Department of Diagnostic Radiology, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan, R.O.C.
Background/Aim:
The administration of contrast agents can adversely affect kidney function. Nevertheless, the nephrotoxicity of iopromide in human renal cells, potential therapeutic agents, and the underlying molecular mechanisms have not been thoroughly investigated.
Materials And Methods:
The proliferation of HEK-293 kidney cells was assessed using the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazoliumbromide (MTT) assay. Apoptotic cell death was examined using the TUNEL assay and caspase-3 activity measurements. The impacts and potential pathways of epigallocatechin-3-gallate (EGCG) on iopromide-induced renal damage were analyzed through whole transcriptome sequencing. The redox state was assessed by measuring reactive oxygen species (ROS) production and 2,2-Diphenyl-1-picrylhydrazyl (DPPH) radical scavenging activity.
Results:
Iopromide-induced inhibition of cell proliferation and apoptosis in HEK-293 cells was counteracted by EGCG co-treatment. Pathway analysis revealed that molecules related to antioxidant and anti-inflammatory responses, such as ERK1/2, STAT1, and NF-[Formula: see text]B, were pivotal in the action of EGCG.
Conclusion:
Iopromide-induced ROS production, decreased DPPH scavenging ability, DNA strand breaks, elevated caspase-3 activity, and reduced cell proliferation were all reversed by EGCG co-treatment in HEK-293 cells. The mechanisms likely involve the attenuation of oxidative stress, inflammatory responses, and apoptosis, with regulation through the ERK1/2, STAT1, and NF-[Formula: see text]B pathways. Further research is necessary to confirm the protective effects of EGCG on renal function, particularly against damage induced by contrast agents like iopromide.
Insights
Epigallocatechin-3-gallate (EGCG) protects human kidney cells from iopromide-induced damage by reducing oxidative stress and apoptosis. This study investigates EGCG
Area of Science:
- Nephrology
- Molecular Biology
- Pharmacology
Background:
- Contrast agents can harm kidney function.
- Iopromide's nephrotoxicity and protective agents are understudied.
Purpose of the Study:
- Investigate iopromide's effects on human renal cells.
- Evaluate epigallocatechin-3-gallate (EGCG) as a potential therapeutic agent.
- Elucidate molecular mechanisms of EGCG's protective action.
Main Methods:
- HEK-293 cell proliferation assay (MTT).
- Apoptosis assessment (TUNEL assay, caspase-3 activity).
- Whole transcriptome sequencing for pathway analysis.
- Redox state evaluation (ROS, DPPH assay).
Main Results:
- EGCG counteracted iopromide-induced cell proliferation inhibition and apoptosis.
- Pathway analysis identified antioxidant and anti-inflammatory molecules (ERK1/2, STAT1, NF-κB) crucial for EGCG's effects.
Conclusions:
- EGCG reversed iopromide-induced oxidative stress, DNA damage, and apoptosis in HEK-293 cells.
- Mechanisms involve attenuating oxidative stress, inflammation, and apoptosis via ERK1/2, STAT1, and NF-κB pathways.
- Further research is needed to confirm EGCG's renal protective effects against contrast agent-induced damage.
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