Targeting the Nrf2ARE Signalling Pathway to Mitigate Isoproterenol-Induced Cardiac Hypertrophy: Plausible Role of Hesperetin in Redox Homeostasis
Joint Authors
Velusamy, Prema
Srinivasan, Ashokkumar
Mohan, Thangarajeswari
Ravi, Divya Bhavani
Periandavan, Kalaiselvi
Singh, Abhilasha
Chakrapani, Lakshmi Narasimhan
Kishore Kumar, S. N.
Varadharaj, Saradhadevi
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2020, Issue 2020 (31 Dec. 2020), pp.1-13, 13 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2020-09-01
Country of Publication
Egypt
No. of Pages
13
Main Subjects
Abstract EN
Cardiac hypertrophy is the underlying cause of heart failure and is characterized by excessive oxidative stress leading to collagen deposition.
Therefore, understanding the signalling mechanisms involved in excessive extracellular matrix deposition is necessary to prevent cardiac remodelling and heart failure.
In this study, we hypothesized that hesperetin, a flavanone that elicits the activation of Nrf2 signalling and thereby suppresses oxidative stress, mediated pathological cardiac hypertrophy progression.
A cardiac hypertrophy model was established with subcutaneous injection of isoproterenol in male Wistar rats.
Oxidative stress markers, antioxidant defense status, and its upstream signalling molecules were evaluated to discover the impacts of hesperetin in ameliorating cardiac hypertrophy.
Our results implicate that hesperetin pretreatment resulted in the mitigation of oxidative stress by upregulating antioxidant capacity of the heart.
This curative effect might be owing to the activation of the master regulator of antioxidant defense system, known as Nrf2.
Further, analysis of Nrf2 revealed that hesperetin enhances its nuclear translocation as well as the expression of its downstream targets (GCLC, NQO1, and HO-1) to boost the antioxidative status of the cells.
To support this notion, in vitro studies were carried out in isoproterenol-treated H9c2 cells.
Immunocytochemical analysis showed augmented nuclear localization of Nrf2 implicating the action of hesperetin at the molecular level to maintain the cellular redox homeostasis.
Thus, it is conceivable that hesperetin could be a potential therapeutic candidate that enhances Nrf2 signalling and thereby ameliorates pathological cardiac remodelling.
American Psychological Association (APA)
Velusamy, Prema& Mohan, Thangarajeswari& Ravi, Divya Bhavani& Kishore Kumar, S. N.& Srinivasan, Ashokkumar& Chakrapani, Lakshmi Narasimhan…[et al.]. 2020. Targeting the Nrf2ARE Signalling Pathway to Mitigate Isoproterenol-Induced Cardiac Hypertrophy: Plausible Role of Hesperetin in Redox Homeostasis. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-13.
https://search.emarefa.net/detail/BIM-1206088
Modern Language Association (MLA)
Velusamy, Prema…[et al.]. Targeting the Nrf2ARE Signalling Pathway to Mitigate Isoproterenol-Induced Cardiac Hypertrophy: Plausible Role of Hesperetin in Redox Homeostasis. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-13.
https://search.emarefa.net/detail/BIM-1206088
American Medical Association (AMA)
Velusamy, Prema& Mohan, Thangarajeswari& Ravi, Divya Bhavani& Kishore Kumar, S. N.& Srinivasan, Ashokkumar& Chakrapani, Lakshmi Narasimhan…[et al.]. Targeting the Nrf2ARE Signalling Pathway to Mitigate Isoproterenol-Induced Cardiac Hypertrophy: Plausible Role of Hesperetin in Redox Homeostasis. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-13.
https://search.emarefa.net/detail/BIM-1206088
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1206088