Cardioprotective potential of Fridericia platyphylla (Cham.) L.G. Lohmann: Phytochemical characterization and experimental evidence.

BACKGROUND

The isoproterenol (ISO)-induced myocardial injury (MI) model is widely used to investigate cardioprotective strategies in the context of sustained β-adrenergic overstimulation, oxidative stress, and disruption of calcium homeostasis. Plant-derived products rich in phenolic compounds have attracted interest due to their antioxidant, anti-inflammatory, and cytoprotective properties. Fridericia platyphylla (Cham.) L.G. Lohmann is a medicinal species traditionally recognized as a source of bioactive compounds and represents a promising candidate for experimental cardioprotection.

PURPOSE: To characterize the phytochemical profile of a hydroethanolic extract of F. platyphylla (FPE) and evaluate its cardioprotective effects and dose-related responses in an ISO-induced MI model.

METHODS

Phytochemical characterization was performed using LC-MS/MS, enabling the annotation of phenolic acids and flavonoids. Male Wistar rats were orally treated with FPE at different doses for 15 days, followed by ISO-induced myocardial injury. Hemodynamic and electrocardiographic parameters were recorded. Biochemical markers of cardiac injury, systemic biochemical and hematological parameters, coagulation indices, infarct size, cardiac hypertrophy, and histopathological alterations were assessed.

RESULTS

LC-MS/MS identified rutin as the major constituent in a phenolic-rich profile. FPE treatment conferred dose-related cardioprotection, with more pronounced effects at doses of 75 and 100 mg/kg in the ISO-induced MI model. FPE restored electrocardiographic alterations, reduced infarct size, attenuated cardiac hypertrophy, decreased circulating cardiac injury markers, and mitigated collagen deposition. Additionally, FPE improved hematological parameters and reduced plasma fibrinogen levels, indicating anti-inflammatory and antithrombotic effects.

CONCLUSIONS

FPE treatment for 15 days produced dose-dependent cardioprotective effects against ISO-induced MI, reinforcing its pharmacological potential as a source of bioactive compounds for experimental cardioprevention.