Bibliographic Details
| Title: |
Cardioprotective Effect of Taxifolin against Isoproterenol-Induced Cardiac Injury through Decreasing Oxidative Stress, Inflammation, and Cell Death, and Activating Nrf2/HO-1 in Mice. |
| Authors: |
Obeidat, Heba M.1 (AUTHOR), Althunibat, Osama Y.1 (AUTHOR), Alfwuaires, Manal A.2 (AUTHOR), Aladaileh, Saleem H.1,3 (AUTHOR), Algefare, Abdulmohsen I.2 (AUTHOR), Almuqati, Afaf F.4 (AUTHOR), Alasmari, Fawaz5 (AUTHOR), Aldal'in, Hammad Khalifeh6 (AUTHOR), Alanezi, Abdulkareem A.7 (AUTHOR), Alsuwayt, Bader3 (AUTHOR), Abukhalil, Mohammad H.1,8 (AUTHOR) mabukhalil@ahu.edu.jo |
| Source: |
Biomolecules (2218-273X). Nov2022, Vol. 12 Issue 11, p1546. 16p. |
| Subject Terms: |
*CELL death, *HEART injuries, *OXIDATIVE stress, *MYOCARDIAL injury, *TROPONIN I, *PYROPTOSIS |
| Abstract: |
Oxidative stress and inflammation are key components in cardiovascular diseases and heart dysfunction. Herein, we evaluated the protective effects of (+)-taxifolin (TAX), a potent flavonoid with significant antioxidant and anti-inflammatory actions, on myocardial oxidative tissue injury, inflammation, and cell death, using a mouse model of isoproterenol (ISO)-induced acute myocardial injury. Mice were given TAX (25 and 50 mg/kg, orally) for 14 days before receiving two subsequent injections of ISO (100 mg/kg, s.c.) at an interval of 24 h on the 15th and 16th days. The ISO-induced cardiac tissue injury was evidenced by increased serum creatine kinase-MB (CK-MB), cardiac troponin I (cTnI), and lactate dehydrogenase (LDH), along with several histopathological changes. The ISO also induced increased malondialdehyde (MDA) with concomitant declined myocardial glutathione level and antioxidant enzymes activities. Moreover, ISO-induced heart injury was accompained with elevated cardiac NF-κB p65, TNF-α, IL-1β, Bax, and caspase-3, as well as decreased Bcl-2, Nrf2, and HO-1. Remarkably, TAX reduced the severity of cardiac injury, oxidative stress, inflammation, and cell death, while enhancing antioxidants, Bcl-2, and Nrf2/HO-1 signaling in ISO-injected mice. In conclusion, TAX protects against ISO-induced acute myocardial injury via activating the Nrf2/HO-1 signaling pathway and attenuating the oxidative tissue injury and key regulators of inflammatory response and apoptosis. Thus, our findings imply that TAX may constitute a new cardioprotective therapy against acute MI, which undoubtedly deserves further exploration in upcoming human trials. [ABSTRACT FROM AUTHOR] |
|
Copyright of Biomolecules (2218-273X) is the property of MDPI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) |
| Database: |
Academic Search Complete |
|
Full text is not displayed to guests. |
Login for full access.
|
