Astaxanthin Protects Ochratoxin A-Induced Oxidative Stress and Apoptosis in the Heart via the Nrf2 Pathway
| Autor: | Beibei Yao, Mingyang Wang, Danyang Jiao, Ketao Xu, Weixiang Xu, Yueli Chen, Yang Guo, Shuhua Yang, Gengyuan Cui, Miao Long, Lin Li, Peng Li |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
Male
Aging Antioxidant medicine.medical_treatment Apoptosis Xanthophylls medicine.disease_cause Biochemistry Antioxidants chemistry.chemical_compound Electrocardiography Heart Rate Myocytes Cardiac bcl-2-Associated X Protein Kelch-Like ECH-Associated Protein 1 medicine.diagnostic_test biology Caspase 3 General Medicine Organ Size Malondialdehyde Ochratoxins Caspase 9 Mitochondria Research Article Signal Transduction medicine.medical_specialty Cardiotonic Agents Article Subject NF-E2-Related Factor 2 Protective Agents Superoxide dismutase Western blot Internal medicine Lactate dehydrogenase medicine Animals QH573-671 Myocardium Body Weight Cell Biology Glutathione Mice Inbred C57BL Oxidative Stress Endocrinology chemistry biology.protein Creatine kinase Cytology Oxidative stress |
| Zdroj: | Oxidative Medicine and Cellular Longevity Oxidative Medicine and Cellular Longevity, Vol 2020 (2020) |
| ISSN: | 1942-0994 1942-0900 |
| Popis: | This study assessed the protective mechanism of astaxanthin (ASX) against ochratoxin A- (OTA-) induced cardiac injury in mice. Four groups of mice were established: control group (0.1 mL olive oil+0.1 mL NaHCO2), OTA group (0.1 mL OTA 5 mg/kg body weight), ASX group (0.1 mL ASX 100 mg/kg body weight), and ASX + OTA group (0.1 mL ASX 100 mg/kg body weight, 2 h later, 0.1 mL OTA 5 mg/kg body weight). The test period lasted for 27 days (7 days of dosing, 2 days of rest). Electrocardiogram, body weight, heart weight, tissue pathology, oxidative markers (malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH)), biochemical markers (creatine kinase (CK), creatine kinase isoenzyme (CK-MB), and lactate dehydrogenase (LDH)), electron microscopy, TUNEL, and Western blot tests were used to examine the effects of OTA on myocardial injury and ASX detoxification. The results showed that OTA exposure significantly decreased both body weight and heart weight. OTA induced a decrease in heart rate in mice and decreased tissue concentrations of SOD, CAT, and GSH, while increasing serum concentrations of cardiac enzymes (CK, CK-MB, and LDH) and tissue MDA. ASX improved heart rate, cardiac enzymes, and antioxidant levels in mice. The results of tissue pathology and TUNEL assay showed that ASX protects against OTA-induced myocardial injury. In addition, Western blot results showed that the OTA group upregulated Keap1, Bax, Caspase3, and Caspase9, while it downregulated Nrf2, HO-1, and Bcl-2 protein expression. ASX played a protective role by changing the expression of Keap1, Nrf2, HO-1, Bax, Bcl-2, Caspase3, and Caspase9 proteins. These results indicate that the protective mechanism of ASX on the myocardium works through the Keap1-Nrf2 signaling pathway and mitochondria-mediated apoptosis pathway. This study provides a molecular rationale for the mechanism underlying OTA-induced myocardial injury and the protective effect of ASX on the myocardium. |
| Databáze: | OpenAIRE |
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