黄芪甲苷对微波辐射所致心脏损伤的保护作用及其机制。

IF 2.5 3区 医学 Q2 BIOLOGY
Xueyan Zhang, Li Zhao, Shaohua Hu, Congcong Miao, Ji Dong, Jing Zhang, Binwei Yao, Yan Lv, Ruiyun Peng
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引用次数: 0

摘要

本研究探讨黄芪甲苷(astragaloside, AST)对微波辐射致心脏损伤的潜在保护作用及其机制。采用s波段微波辐照大鼠和H9c2细胞,建立离体和体内心脏损伤模型。AST给药7 d和/或14 d后进行电生理检查、血清生化分析、苏木精伊红(H&E)染色、透射电镜(TEM)、western blot、免疫组织化学染色等实验。对经1-Azakenpaullone(糖原合成酶激酶3β抑制剂)或AST预处理的辐照H9c2细胞,进行TEM、细胞计数试剂盒-8、western blot、四甲基罗丹明甲基lester染色、活性氧(ROS)、三磷酸腺苷(ATP)和线粒体膜电位(MMP)测定等实验。体内实验结果显示,暴露后第7天,微波辐射引起了严重的心脏损伤(表现为心电图和心脏组织结构异常,血清心肌酶活性和Ca2+浓度升高),糖原合成酶激酶3β (p-GSK-3βSer9)磷酸化水平降低。经AST治疗后,这些变化均逆转。体外实验结果表明,微波辐射导致H9c2细胞p-GSK-3βSer9水平降低,线粒体通透性过渡孔(mPTP)开口增加,线粒体功能障碍加重(细胞内ROS生成增加,细胞内ATP合成减少,MMP下降)。经1-Azakenpaullone和AST预处理后,这些变化均被逆转。提示AST可通过促进GSK-3βSer9磷酸化,抑制mPTP开放,恢复线粒体功能,从而保护微波辐射诱导的心脏损伤。本研究为减轻微波辐射对心脏健康的不良影响提供了有价值的潜在治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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.

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来源期刊
Radiation research
Radiation research 医学-核医学
CiteScore
5.10
自引率
8.80%
发文量
179
审稿时长
1 months
期刊介绍: Radiation Research publishes original articles dealing with radiation effects and related subjects in the areas of physics, chemistry, biology and medicine, including epidemiology and translational research. The term radiation is used in its broadest sense and includes specifically ionizing radiation and ultraviolet, visible and infrared light as well as microwaves, ultrasound and heat. Effects may be physical, chemical or biological. Related subjects include (but are not limited to) dosimetry methods and instrumentation, isotope techniques and studies with chemical agents contributing to the understanding of radiation effects.
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