Protective Effects and Mechanisms of Astragaloside on Microwave Radiation-induced Cardiac Injury

This study explores the potential protective effects and mechanisms of astragaloside (AST) on microwave radiation-induced cardiac injury. Rats and H9c2 cells were irradiated with S-band microwave to induce in vivo and in vitro cardiac injury models. In irradiated rats, experiments such as electrophysiological examination, serum biochemical analysis, hematoxylin and eosin (H&E) staining, transmission electron microscopy (TEM), western blot, and immunohistochemical staining were performed after AST were administrated for 7 and/or 14 days. In irradiated H9c2 cells that were pretreated with 1-Azakenpaullone (glycogen synthase kinase-3β inhibitor) or AST, experiments such as TEM, cell counting kit-8 assay, western blot, tetramethylrhodamine methylester staining, and determination of reactive oxygen species (ROS), adenosine triphosphate (ATP) and mitochondrial membrane potential (MMP) were performed. In vivo results showed that at 7 days after exposure, microwave radiation-induced severe cardiac injury (as evidenced by abnormal electrocardiograms and cardiac tissue structure, increased serum myocardial enzyme activities and Ca2+ concentration) and lower level of phosphorylation of glycogen synthase kinase-3β (p-GSK-3βSer9). All these changes were reversed after AST treatment. The results of in vitro experiments showed that microwave radiation induced a lower level of p-GSK-3βSer9, more mitochondrial permeability transition pore (mPTP) opening and more serious mitochondrial dysfunction (characterized by increased intracellular ROS production, decreased intracellular ATP synthesis and MMP decline) in H9c2 cells. All these changes were reversed by 1-Azakenpaullone and AST pretreatment. The findings suggest that AST could shield against microwave radiation-induced cardiac injury by promoting the phosphorylation of GSK-3βSer9, thereby inhibiting mPTP opening and restoring mitochondrial function. This study offers valuable insights into potential therapeutic strategies for mitigating the adverse effects of microwave radiation on cardiac health.

Authors

Institutions

Publication Details

Journal
Radiation Research
Published
2025-02-06
DOI
https://doi.org/10.1667/rade-23-00103.1
Citations
1
Primary Topic
Cardiac Ischemia and Reperfusion
Type
article
Field-Weighted Citation Impact
1.47
Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Protective Effects and Mechanisms of Astragaloside on Microwave Radiation-induced Cardiac Injury

Ji Dong, Congcong Miao, Li Zhao, Shaohua Hu et al.
1 citations
Radiation Research
Cardiac Ischemia and Reperfusion
1.47
article

Protective Effects and Mechanisms of Astragaloside on Microwave Radiation-induced Cardiac Injury

Ji Dong, Congcong Miao, Li Zhao, Shaohua Hu, Jing Zhang, Xueyan Zhang, Peng Ruiyun, Binwei Yao, Yan Lv
article en
1 citations

Abstract

This study explores the potential protective effects and mechanisms of astragaloside (AST) on microwave radiation-induced cardiac injury. Rats and H9c2 cells were irradiated with S-band microwave to induce in vivo and in vitro cardiac injury models. In irradiated rats, experiments such as electrophysiological examination, serum biochemical analysis, hematoxylin and eosin (H&E) staining, transmission electron microscopy (TEM), western blot, and immunohistochemical staining were performed after AST were administrated for 7 and/or 14 days. In irradiated H9c2 cells that were pretreated with 1-Azakenpaullone (glycogen synthase kinase-3β inhibitor) or AST, experiments such as TEM, cell counting kit-8 assay, western blot, tetramethylrhodamine methylester staining, and determination of reactive oxygen species (ROS), adenosine triphosphate (ATP) and mitochondrial membrane potential (MMP) were performed. In vivo results showed that at 7 days after exposure, microwave radiation-induced severe cardiac injury (as evidenced by abnormal electrocardiograms and cardiac tissue structure, increased serum myocardial enzyme activities and Ca2+ concentration) and lower level of phosphorylation of glycogen synthase kinase-3β (p-GSK-3βSer9). All these changes were reversed after AST treatment. The results of in vitro experiments showed that microwave radiation induced a lower level of p-GSK-3βSer9, more mitochondrial permeability transition pore (mPTP) opening and more serious mitochondrial dysfunction (characterized by increased intracellular ROS production, decreased intracellular ATP synthesis and MMP decline) in H9c2 cells. All these changes were reversed by 1-Azakenpaullone and AST pretreatment. The findings suggest that AST could shield against microwave radiation-induced cardiac injury by promoting the phosphorylation of GSK-3βSer9, thereby inhibiting mPTP opening and restoring mitochondrial function. This study offers valuable insights into potential therapeutic strategies for mitigating the adverse effects of microwave radiation on cardiac health.

Radiation ResearchVol. 203(3)
Capital Medical University (CN), Academy of Military Medical Sciences (CN), Shanghai Stomatological Hospital (CN), Shanghai Children's Hospital (CN)
Good health and well-being
Openalex Percentile: Top 23%
Cardiac Ischemia and Reperfusion
1.47
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.