Hesperidin regresses cardiac hypertrophy by virtue of PPAR‐γ agonistic, anti‐inflammatory, antiapoptotic, and antioxidant properties

• Published in: Journal of biochemical and molecular toxicology Vol. 33; no. 5; pp. e22283 - n/a
• Main Authors: Bhargava, Poorva, Verma, Vipin Kumar, Malik, Salma, Khan, Sana Irfan, Bhatia, Jagriti, Arya, Dharamvir Singh
• Format: Journal Article
• Language: English
• Published: United States Wiley Subscription Services, Inc 01-05-2019
• Subjects: Animals; Anti-Inflammatory Agents - pharmacology; Antioxidants; Antioxidants - pharmacology; Apoptosis; Apoptosis - drug effects; cardiac hypertrophy (CH); Cardiomegaly - chemically induced; Cardiomegaly - metabolism; Cardiomegaly - prevention & control; Cardiotonic Agents - pharmacology; Citrus fruits; Gene Expression Regulation - drug effects; Heart; Hemodynamics; Hesperidin; hesperidin (HES); Hesperidin - pharmacology; Hypertrophy; Inflammation; Isoproterenol; isoproterenol (ISO); Isoproterenol - adverse effects; Isoproterenol - pharmacology; Male; Oxidative stress; Oxidative Stress - drug effects; Peroxisome proliferator-activated receptors; peroxisome proliferator‐activated receptor gamma (PPAR‐γ); PPAR gamma - agonists; PPAR gamma - biosynthesis; Rats; Rats, Wistar; Rodents; hesperidin (HES); inflammation; peroxisome proliferator-activated receptor gamma (PPAR-γ); isoproterenol (ISO); oxidative stress; cardiac hypertrophy (CH)
• ISSN: 1095-6670; 1099-0461
• DOI: 10.1002/jbt.22283

Hesperidin (HES), a flavanone glycoside, predominant in citrus fruits, has an agonistic activity on peroxisome proliferator‐activated receptor gamma (PPAR‐γ). PPAR‐γ is an inhibitor of cardiac hypertrophy (CH) signaling pathways. In this study, we investigated the cardioprotective effect of HES in isoproterenol (ISO)‐induced CH through PPAR‐γ agonistic activity. For this, male albino Wistar rats were divided into six groups (n = 6), that is, normal, ISO‐control, HES treatment group (200 mg kg−1; p.o.), HES per se (200 mg kg−1; p.o.), enalapril treatment group (30 mg kg−1; p.o.), and combination group (HES 200 mg kg−1; p.o.+enalapril 30 mg kg−1; p.o.). ISO (3 mg kg−1; s.c.) was administered to all groups except normal and per se to induce CH. HES or enalapril treatment of 28 days significantly attenuated pathological changes, improved cardiac hemodynamics, suppressed oxidative stress, and apoptosis along with an increased PPAR‐γ expression. The combination of enalapril with HES exhibited an effect similar to that of HES or enalapril alone on all the aforementioned parameters. Therefore, HES may be further evaluated as a promising molecule for the alleviation of CH.