Artemisia argyi mitigates doxorubicin-induced cardiotoxicity by inhibiting mitochondrial dysfunction through the IGF-IIR/Drp1/GATA4 signaling pathway.

Autor: Chen JK; Department of Chinese Medicine, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.; Integration Center of Traditional Chinese and Modern Medicine, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.; Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan., Ramesh S; Cardiovascular and Mitochondrial Related Disease Research Center, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.; Department of Research and Innovation, Institute of Biotechnology, Saveetha School of Engineering (SSE), Saveetha Institute of Medical and Technical Sciences (SIMATS), Chennai, India., Islam MN; Cardiovascular and Mitochondrial Related Disease Research Center, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan., Shibu MA; Department of Biotechnology, Bharathiar University, Coimbatore, India., Kuo CH; Laboratory of Exercise Biochemistry, University of Taipei, Taipei, Taiwan., Hsieh DJ; School of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung, Taiwan.; Clinical Laboratory, Chung Shan Medical University Hospital, Taichung, Taiwan., Lin SZ; Bioinnovation Center, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.; Department of Neurosurgery, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan., Kuo WW; Department of Biological Science and Technology, College of Life Sciences, China Medical University, Taichung, Taiwan.; Ph.D. Program for Biotechnology Industry, China Medical University, Taichung, Taiwan.; School of Pharmacy, China Medical University, Taichung, Taiwan., Huang CY; Cardiovascular and Mitochondrial Related Disease Research Center, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.; Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan.; Department of Medical Research, China Medical University Hospital, China Medical University, Taichung, Taiwan.; Department of Medical Laboratory Science and Biotechnology, Asia University, Taichung, Taiwan.; Center of General Education, Buddhist Tzu Chi Medical Foundation, Tzu Chi University, Hualien, Taiwan., Ho TJ; Department of Chinese Medicine, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.; Integration Center of Traditional Chinese and Modern Medicine, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.; Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan.; School of Post-Baccalaureate Chinese Medicine, College of Medicine, Tzu Chi University, Hualien, Taiwan.
Jazyk: angličtina
Zdroj: Biotechnology and applied biochemistry [Biotechnol Appl Biochem] 2024 Oct 07. Date of Electronic Publication: 2024 Oct 07.
DOI: 10.1002/bab.2671
Abstrakt: Doxorubicin (DOX) is mostly utilized as a wide range of antitumor anthracycline to treat different cancers. The severe antagonistic impacts of DOX on cardiotoxicity constrain its clinical application. Many mechanisms are involved in cardiac toxicity induced by DOX in the human body. Mitochondria is a central part of fatty acid and glucose metabolism. Thus, impaired mitochondrial metabolism can increase heart failure risk, which can play a vital role in cardiomyocyte mitochondrial dysfunction. This study aimed to assess the possible cardioprotective effect of water-extracted Artemisia argyi (AA) against the side effect of DOX in H9c2 cells and whether these protective effects are mediated through IGF-IIR/Drp1/GATA4 signaling pathways. Although several studies proved that AA extract has benefits for various diseases, its cardiac effects have not yet been identified. The H9c2 cells were exposed to 1 μM to establish a model of cardiac toxicity. The results revealed that water-extracted AA could block the expression of IGF-IIR/calcineurin signaling pathways induced by DOX. Notably, our results also showed that AA treatment markedly attenuated Akt phosphorylation and cleaved caspase 3, and the nuclear translocation markers NFATC3 and p-GATA4. Using actin staining for hypertrophy, we determined that AA can reduce the effect of mitochondrial reactive oxygen species and cell size. These findings suggest that water-extracted AA could be a suitable candidate for preventing DOX-induced cardiac damage.
(© 2024 International Union of Biochemistry and Molecular Biology, Inc.)
Databáze: MEDLINE
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