Hydrogen Attenuates Thyroid Hormone-Induced Cardiac Hypertrophy in Rats by regulating angiotensin II type 1 receptor and NADPH oxidase 2 mediated oxidative stress.
Hongxiao Yang, Juncai Bai, Chengchuang Zhan, Shuang Liu, Yunan Gao, Lihua Zhong, Yajing Lv, Jing Chi, Jiaren Liu, Xinrui Yang, Wei Yang · European journal of pharmacology · 2022
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Independent study record
Each H2HUBB study page organizes source-linked research details for educational use. Interpretation should remain proportional to the study design, population, controls, and limitations.
H2HUBB TAKEAWAY
In rats, hydrogen treatment also reduced the levothyroxine-induced increase in cardiac malondialdehyde, 8-hydroxy-2-deoxyguanosine and serum hydrogen peroxide levels and upregulated superoxide dismutase and glutathione peroxidase activity. These results are preclinical and suggest molecular hydrogen's therapeutic potential in the condition studied. Further human research is needed to establish clinical effectiveness. This was a preclinical rat study of molecular hydrogen. Oxidative-stress and peroxide-related terminology describes the measured pathway rather than the administered intervention, and the findings cannot be assumed to establish human effectiveness.
What the Researchers Studied
The study examined rats.
How Molecular Hydrogen Was Used
Hydrogen is a good antioxidant. hydrogen inhalation ameliorated the levothyroxine-induced metabolic increase and cardiac hypertrophy in rats. Serum brain natriuretic peptide expression was also attenuated by hydrogen treatment.
What the Researchers Found
Hydrogen inhalation ameliorated the levothyroxine-induced metabolic increase and cardiac hypertrophy in rats. However, hydrogen had no significant effect on levothyroxine -induced serum troponin I and serum thyroid hormone changes. Hydrogen treatment also reduced the levothyroxine-induced increase in cardiac malondialdehyde, 8-hydroxy-2-deoxyguanosine and serum hydrogen peroxide levels and upregulated superoxide dismutase and glutathione peroxidase activity.
H₂ Mechanisms / Biological Findings
, the present study revealed a protective effect of hydrogen on levothyroxine -induced cardiac hypertrophy by regulating angiotensin II type 1 receptors and NOX2-mediated oxidative stress in rats. western blotting results showed that hydrogen inhalation inhibited the expression of cardiac nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2), angiotensin II type 1 receptor, sarcoplasmic reticulum Ca2+-ATPase (SERCA2), phospho-phospholamban and α-myosin heavy chain proteins.
Authors’ Conclusion
The authors concluded that , the present study revealed a protective effect of hydrogen on levothyroxine -induced cardiac hypertrophy by regulating angiotensin II type 1 receptors and NOX2-mediated oxidative stress in rats.
H2HUBB Evidence Boundary
This was a preclinical rat study of molecular hydrogen. Oxidative-stress and peroxide-related terminology describes the measured pathway rather than the administered intervention, and the findings cannot be assumed to establish human effectiveness.