Phyllanthin from Phyllanthus amarus protects the myocardium during pressure overload-induced cardiac hypertrophy by inhibiting the angiotensin-converting enzyme.

Ischemic heart disease results from obstruction of blood flow and leads to myocardial infarction. Various lignans of herbal origin have been shown to protect against cardiotoxicity. The present study aimed to assess the poten-tial of phyllanthin, identified from a standardized methanolic extract of Phyl-lanthus amarus (PAME), against pressure overload-induced cardiac hypertrophy in experimental rats. Lignan was identified in PAME usingHPLC. Ligating the abdominal aorta induced cardiac hypertrophy in Wistar rats (220-240g). Then they were treated with (n=15, each) either distilled water (10 mL/kg, aortic stenosis control), lisinopril (15 mg/kg), or PAME(50, 100 and 200 mg/kg) for 28 days. Lignan compounds were identified using UV spectra in PAME, and HPLC analysis showed the presence of phyllanthin at 25.30 retention time with an area of 70.22%. Treatment with PAME (100 and 200 mg/kg) significantly and dose-de-pendently (p<0.01 and p<0.001) ameliorated AS-induced elevation in absolute and relative heart weights, increased serum biomarker levels, and alterations in electrocardiographic and hemodynamic functions. PAME effectively inhibited AS-induced oxide-nitrosative stress dose-dependently (p<0.01 and p<0.001). Up-regulated mRNA expression of cardiac angiotensin-converting enzyme (ACE) and Collagen-I were also markedly inhibited (p<0.01 and p<0.001) by PAME. Fur-thermore, PAME significantly reduced (p<0.01 and p<0.001) pressure overload-induced alterations in cardiac histopathology. In conclusion, phyllanthin identi-fied from P. amarus ameliorated pressure overload-induced cardiac hypertrophy by inhibiting ACE and collagen-I formation pathways to alleviate hypertension and fibrosis. These findings collectively suggest that P. amarus represents prom-ising therapy for managing ischemic heart diseases.