Rhodiola and Salidroside Attenuate Oxidative Stress-Triggered H9c2 Cardiomyoblast Apoptosis Through IGF1R-Induced ERK1/2 Activation.

Autor: Ju IJ; Division of General Medicine, Department of Medical Education, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.; Department of Neurological Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan., Tsai BC; Cardiovascular and Mitochondrial Related Disease Research Center, 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., Kuo CH; Laboratory of Exercise Biochemistry, University of Taipei, Taipei, Taiwan.; Institute of Sports Sciences, University of Taipei, Taipei, Taiwan.; Department of Kinesiology and Health Science, College of William and Mary, Williamsburg, VA, USA.; School of Physical Education and Sports Science, Soochow University, Suzhou, Jiangsu, China., Lin YM; Department of Pathology, Changhua Christian Hospital, Changhua, Taiwan.; School of Medicine, Chung Shan Medical University, Taichung, Taiwan., Hsieh DJ; School of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung, Taiwan.; Clinical Laboratory, Chung Shan Medical University Hospital, Taichung, Taiwan., Pai PY; Division of Cardiovascular Medicine, Department of Internal Medicine, China Medical University Hospital, Taichung, Taiwan.; School of Medicine, College of Medicine, China Medical University, Taichung, Taiwan., Huang SE; Cardiovascular and Mitochondrial Related Disease Research Center, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.; Graduate Institute of Chinese Medicine, China Medical University, Taichung, Taiwan., Lu SY; Division of Cardiovascular Medicine, Department of Internal Medicine, China Medical University Hospital, Taichung, Taiwan.; School of Medicine, College of Medicine, China Medical University, Taichung, Taiwan.; Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan., Lee SD; School of Rehabilitation Science, Shanghai University of Traditional Chinese Medicine, Shanghai, China.; School of Rehabilitation Medicine, Weifang Medical University, Weifang, Shandong, China.; Department of Physical Therapy, Graduate Institute of Rehabilitation Science, 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 of Science and Technology, Hualien, Taiwan.
Jazyk: angličtina
Zdroj: Environmental toxicology [Environ Toxicol] 2024 Nov; Vol. 39 (11), pp. 5150-5161. Date of Electronic Publication: 2024 Aug 07.
DOI: 10.1002/tox.24372
Abstrakt: Oxidative stress is a pivotal factor in the pathogenesis of various cardiovascular diseases. Rhodiola, a traditional Chinese medicine, is recognized for its potent antioxidant properties. Salidroside, a phenylpropanoid glycoside derived from Rhodiola rosea, has shown remarkable antioxidant capabilities. This study aimed to elucidate the potential protective mechanisms of Rhodiola and salidroside against H 2 O 2 -induced cardiac apoptosis in H9c2 cardiomyoblast cells. H9c2 cells were exposed to H 2 O 2 for 4 h, and subsequently treated with Rhodiola or salidroside for 24 h. Cell viability and apoptotic pathways were assessed. The involvement of insulin-like growth factor 1 receptor (IGF1R) and the activation of extracellular regulated protein kinases 1/2 (ERK1/2) were investigated. H 2 O 2 (100 μM) exposure significantly induced cardiac apoptosis in H9c2 cells. However, treatment with Rhodiola (12.5, 25, and 50 μg/mL) and salidroside (0.1, 1, and 10 nM) effectively attenuated H 2 O 2 -induced cytotoxicity and apoptosis. This protective effect was associated with IGF1R-activated phosphorylation of ERK1/2, leading to the inhibition of Fas-dependent proteins, HIF-1α, Bax, and Bak expression in H9c2 cells. The images from hematoxylin and eosin staining and immunofluorescence assays also revealed the protective effects of Rhodiola and salidroside in H9c2 cells against oxidative damage. Our findings suggest that Rhodiola and salidroside possess antioxidative properties that mitigate H 2 O 2 -induced apoptosis in H9c2 cells. The protective mechanisms involve the activation of IGF1R and subsequent phosphorylation of ERK1/2. These results propose Rhodiola and salidroside as potential therapeutic agents for cardiomyocyte cytotoxicity and apoptosis induced by oxidative stress in heart diseases. Future studies may explore their clinical applications in cardiac health.
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Databáze: MEDLINE