3,4-Dihydroxybenzalacetone (DBL) Prevents Aging-Induced Myocardial Changes in Senescence-Accelerated Mouse-Prone 8 (SAMP8) Mice
Aging is a predominant risk factor for the development and progression of cardiovascular complications. Physiologically and anatomically, the heart undergoes numerous changes that result in poor cardiac function in the elderly population. Recently, several studies have provided promising results, co...
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MDPI AG
2020-03-01
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| author | Vijayasree V. Giridharan Vengadeshprabhu Karupppagounder Somasundaram Arumugam Yutaka Nakamura Ashrith Guha Tatiana Barichello Joao Quevedo Kenichi Watanabe Tetsuya Konishi Rajarajan A. Thandavarayan |
| author_facet | Vijayasree V. Giridharan Vengadeshprabhu Karupppagounder Somasundaram Arumugam Yutaka Nakamura Ashrith Guha Tatiana Barichello Joao Quevedo Kenichi Watanabe Tetsuya Konishi Rajarajan A. Thandavarayan |
| author_sort | Vijayasree V. Giridharan |
| collection | DOAJ |
| description | Aging is a predominant risk factor for the development and progression of cardiovascular complications. Physiologically and anatomically, the heart undergoes numerous changes that result in poor cardiac function in the elderly population. Recently, several studies have provided promising results, confirming the ability of the senescence-accelerated mouse-prone 8 (SAMP8) model to accurately model age-related cardiovascular alterations. In this study, using a murine model of senescence, SAMP8, we aimed to investigate the effect of 3,4-dihydroxybenzalacetone (DBL), a catechol-containing phenylpropanoid derivative isolated from <i>Inonotus</i><i> obliquus </i>(Chaga), on cardiac aging.<i> </i>DBL was administered at the doses of 10 mg/kg and 20 mg/kg by oral gavage to SAMP8 mice to examine aging-mediated cardiac changes, such as oxidative DNA damage, oxygen radical antioxidant capacity (ORAC) value, fibrosis, inflammation, and apoptosis. The treatment with DBL at both doses significantly reduced aging-mediated oxidative DNA damage, and simultaneously increased the ORAC value in the SAMP8 assay. Cardiac fibrosis was assessed with Azan-Mallory staining, and the number of cardiac remodeling markers was found to be significantly reduced after the treatment with DBL. We also observed a decrease in cardiomyocyte apoptosis as measured by the terminal transferase-mediated dUTP nick end labeling (TUNEL) staining method and the caspase-3 levels in SAMP8 mice compared with senescence-resistant control (SAMR1) mice. The findings from this study suggest that DBL has a potentially beneficial effect on aging-mediated myocardial alterations. Further studies are warranted to confirm the promising potential of this catechol compound against aging-associated myocardial dysfunction. |
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| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-03-12T19:16:55Z |
| publishDate | 2020-03-01 |
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| spelling | doaj.art-6425c74016394923877d0523003a45752023-08-02T05:28:33ZengMDPI AGCells2073-44092020-03-019359710.3390/cells9030597cells90305973,4-Dihydroxybenzalacetone (DBL) Prevents Aging-Induced Myocardial Changes in Senescence-Accelerated Mouse-Prone 8 (SAMP8) MiceVijayasree V. Giridharan0Vengadeshprabhu Karupppagounder1Somasundaram Arumugam2Yutaka Nakamura3Ashrith Guha4Tatiana Barichello5Joao Quevedo6Kenichi Watanabe7Tetsuya Konishi8Rajarajan A. Thandavarayan9Translational Psychiatry Program, Faillace Department of Psychiatry and Behavioral Sciences, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston, TX 77054, USADepartment of Orthopedics and Rehabilitation, Penn State College of Medicine, 500 University Drive, Hershey, PA 17033, USADepartment of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Niigata University of Pharmacy and Applied Life Sciences, 265-1, Higashijima, Akiha ku, Niigata 956-8603, JapanFaculty of Applied Life Sciences, Faculty of Pharmaceutical Sciences, Niigata University of Pharmacy and Applied Life Sciences Niigata, Niigata 956-8603, JapanDepartment of Cardiology, Houston Methodist Hospital, Houston, TX 77030, USATranslational Psychiatry Program, Faillace Department of Psychiatry and Behavioral Sciences, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston, TX 77054, USATranslational Psychiatry Program, Faillace Department of Psychiatry and Behavioral Sciences, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston, TX 77054, USADepartment of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Niigata University of Pharmacy and Applied Life Sciences, 265-1, Higashijima, Akiha ku, Niigata 956-8603, JapanNiigata University of Pharmacy & Applied Life Sciences (NUPALS), LIAISON R/D Center, Niigata 956-8603, JapanDepartment of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Niigata University of Pharmacy and Applied Life Sciences, 265-1, Higashijima, Akiha ku, Niigata 956-8603, JapanAging is a predominant risk factor for the development and progression of cardiovascular complications. Physiologically and anatomically, the heart undergoes numerous changes that result in poor cardiac function in the elderly population. Recently, several studies have provided promising results, confirming the ability of the senescence-accelerated mouse-prone 8 (SAMP8) model to accurately model age-related cardiovascular alterations. In this study, using a murine model of senescence, SAMP8, we aimed to investigate the effect of 3,4-dihydroxybenzalacetone (DBL), a catechol-containing phenylpropanoid derivative isolated from <i>Inonotus</i><i> obliquus </i>(Chaga), on cardiac aging.<i> </i>DBL was administered at the doses of 10 mg/kg and 20 mg/kg by oral gavage to SAMP8 mice to examine aging-mediated cardiac changes, such as oxidative DNA damage, oxygen radical antioxidant capacity (ORAC) value, fibrosis, inflammation, and apoptosis. The treatment with DBL at both doses significantly reduced aging-mediated oxidative DNA damage, and simultaneously increased the ORAC value in the SAMP8 assay. Cardiac fibrosis was assessed with Azan-Mallory staining, and the number of cardiac remodeling markers was found to be significantly reduced after the treatment with DBL. We also observed a decrease in cardiomyocyte apoptosis as measured by the terminal transferase-mediated dUTP nick end labeling (TUNEL) staining method and the caspase-3 levels in SAMP8 mice compared with senescence-resistant control (SAMR1) mice. The findings from this study suggest that DBL has a potentially beneficial effect on aging-mediated myocardial alterations. Further studies are warranted to confirm the promising potential of this catechol compound against aging-associated myocardial dysfunction.https://www.mdpi.com/2073-4409/9/3/5973,4-dihydroxybenzalacetonesamp8dna damagefibrosisapoptosis |
| spellingShingle | Vijayasree V. Giridharan Vengadeshprabhu Karupppagounder Somasundaram Arumugam Yutaka Nakamura Ashrith Guha Tatiana Barichello Joao Quevedo Kenichi Watanabe Tetsuya Konishi Rajarajan A. Thandavarayan 3,4-Dihydroxybenzalacetone (DBL) Prevents Aging-Induced Myocardial Changes in Senescence-Accelerated Mouse-Prone 8 (SAMP8) Mice Cells 3,4-dihydroxybenzalacetone samp8 dna damage fibrosis apoptosis |
| title | 3,4-Dihydroxybenzalacetone (DBL) Prevents Aging-Induced Myocardial Changes in Senescence-Accelerated Mouse-Prone 8 (SAMP8) Mice |
| title_full | 3,4-Dihydroxybenzalacetone (DBL) Prevents Aging-Induced Myocardial Changes in Senescence-Accelerated Mouse-Prone 8 (SAMP8) Mice |
| title_fullStr | 3,4-Dihydroxybenzalacetone (DBL) Prevents Aging-Induced Myocardial Changes in Senescence-Accelerated Mouse-Prone 8 (SAMP8) Mice |
| title_full_unstemmed | 3,4-Dihydroxybenzalacetone (DBL) Prevents Aging-Induced Myocardial Changes in Senescence-Accelerated Mouse-Prone 8 (SAMP8) Mice |
| title_short | 3,4-Dihydroxybenzalacetone (DBL) Prevents Aging-Induced Myocardial Changes in Senescence-Accelerated Mouse-Prone 8 (SAMP8) Mice |
| title_sort | 3 4 dihydroxybenzalacetone dbl prevents aging induced myocardial changes in senescence accelerated mouse prone 8 samp8 mice |
| topic | 3,4-dihydroxybenzalacetone samp8 dna damage fibrosis apoptosis |
| url | https://www.mdpi.com/2073-4409/9/3/597 |
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