Beta-glucan protects against isoproterenol-induced cardiac remodeling by regulating the ACE-AT1R axis and attenuates cardiac inflammation and apoptosis

Objective: To investigate the cardioprotective effect of beta-glucan against isoproterenol-induced cardiotoxicity in rats, and elucidate the underlying mechanism. Methods: Rats were orally pretreated with beta-glucan (40 mg/kg body weight) for 30 d, and isoproterenol (20 mg/100 g body weight) was ad...

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Bibliographic Details
Published in:Asian Pacific Journal of Tropical Biomedicine
Main Authors: Anitha Roy, Vasantha Mallenahalli Neelakantappa, Jayashree Ganesan, Balakrishnan Ramajayam Asokan, Srinivasan Kulandaivel, V V Sathibabu Uddandrao, Sengottuvelu Singaravel
Format: Article in Journal/Newspaper
Language:English
Published: Wolters Kluwer Medknow Publications 2023
Subjects:
βeta-glucan
isoproterenol
cardiac inflammation
cardiac apoptosis
cardiovascular diseases
heart failure
myocardial infarction
Arctic medicine. Tropical medicine
RC955-962
Biology (General)
QH301-705.5
Arctic
Online Access:https://doi.org/10.4103/2221-1691.385569
https://doaj.org/article/e78fea4f59724dcc90dad908bed95704
Description
Summary:Objective: To investigate the cardioprotective effect of beta-glucan against isoproterenol-induced cardiotoxicity in rats, and elucidate the underlying mechanism. Methods: Rats were orally pretreated with beta-glucan (40 mg/kg body weight) for 30 d, and isoproterenol (20 mg/100 g body weight) was administered on days 31 and 32. The effects of beta-glucan on markers of cardiac injury, hemodynamic changes, production of proinflammatory cytokines, and the corresponding mRNA expressions were evaluated. In addition, histological analysis was performed. Results: Pretreatment with beta-glucan prevented isoproterenol-induced cardiac injury by preserving the structural and functional integrity of the plasma membrane and attenuating the production of proinflammatory cytokines (NF-κB, TNF-α, IL-6, IL-Ιβ, and IFN-γ) in the heart. Moreover, beta-glucan significantly downregulated the mRNA expression of ACE, AT1R, TNF-α, IL-6, NF-κB, caspase-3, TLR-4, and Bax, and upregulated Bcl-2 in the heart. At the same time, pretreatment with beta-glucan alleviated myocardial damage as reflected in a reduction in myonecrosis, edema, and erythrocyte extravasation with almost imperceptible inflammation. Conclusions: Beta-glucan can protect against isoproterenol-induced cardiotoxicity by attenuating cardiac inflammation and apoptosis and regulating the ACE-AT1R axis, thereby preventing cardiac remodeling.

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