Nardosinone protects H9c2 cardiac cells from angiotensin II-induced hypertrophy
| Autor: | Kun Huang, Meng Du, Lu Gao, Wen Shuo Wang, Bo Wang, Kai Huang, Liu Yang, Dan Huang |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
medicine.medical_specialty
Cardiotonic Agents MAP Kinase Signaling System Cell Biomedical Engineering Biology Biochemistry Muscle hypertrophy Cell Line Biomaterials chemistry.chemical_compound Phosphatidylinositol 3-Kinases Internal medicine Genetics medicine Animals RNA Messenger Protein kinase B PI3K/AKT/mTOR pathway Earth-Surface Processes Cell Size Polycyclic Sesquiterpenes Angiotensin II TOR Serine-Threonine Kinases Hypertrophy Rats Endocrinology medicine.anatomical_structure chemistry Cell culture cardiovascular system Phosphorylation Nardosinone Proto-Oncogene Proteins c-akt Sesquiterpenes hormones hormone substitutes and hormone antagonists Myoblasts Cardiac |
| Zdroj: | Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban. 33(6) |
| ISSN: | 1672-0733 |
| Popis: | Pathological cardiac hypertrophy induced by angiotensin II (AngII) can subsequently give rise to heart failure, a leading cause of mortality. Nardosinone is a pharmacologically active compound extracted from the roots of Nardostachys chinensis, a well-known traditional Chinese medicine. In order to investigate the effects of nardosinone on AngII-induced cardiac cell hypertrophy and the related mechanisms, the myoblast cell line H9c2, derived from embryonic rat heart, was treated with nardosinone (25, 50, 100, and 200 μmol/L) or AngII (1 μmol/L). Then cell surface area and mRNA expression of classical markers of hypertrophy were detected. The related protein levels in PI3K/Akt/mTOR and MEK/ERK signaling pathways were examined by Western blotting. It was found that pretreatment with nardosinone could significantly inhibit the enlargement of cell surface area induced by AngII. The mRNA expression of ANP, BNP and β-MHC was obviously elevated in AngII-treated H9c2 cells, which could be effectively blocked by nardosinone at the concentration of 100 μmol/L. Further study revealed that the protective effects of nardosinone might be mediated by repressing the phosphorylation of related proteins in PI3K/Akt and MEK/ERK signaling pathways. It was suggested that the inhibitory effect of nardosinone on Ang II-induced hypertrophy in H9c2 cells might be mediated by targeting PI3K/Akt and MEK/ERK signaling pathways. |
| Databáze: | OpenAIRE |
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