Ganoderic Acid A Attenuates Pathological Cardiac Hypertrophy by Attenuating Inflammatory Responses

Pathological cardiac hypertrophy is an important risk factor for cardiovascular disease. Ganoderic acid A (GAA), the primary bioactive constituent of Ganoderma lucidum (G. lucidum), is known for its stable chemical properties and diverse biological activities. It has been shown to confer protection against myocardial ischemia-reperfusion injury in rat models, potentially through modulating inflammatory responses and inhibiting protein expression linked to both NF-κB and apoptosis pathways. Nevertheless, the role of GAA in cardiac hypertrophy has not yet been fully elucidated. Using transverse aortic constriction (TAC)-induced cardiac hypertrophy in mice, we analyzed the degree of hypertrophy using echocardiography and at the pathology and molecular levels. Our results demonstrate that GAA effectively attenuates Ang II-induced cardiomyocyte hypertrophy in vitro and reduces pressure overload-induced cardiac hypertrophy in vivo. Further investigation revealed that GAA exerts its anti-hypertrophic effects by downregulating the mRNA expression of hypertrophic and fibrotic markers and attenuating inflammatory responses, and that the protective effects of GAA may involve NF-κB signaling. This study provides valuable theoretical support for the potential therapeutic application of GAA in treating pathological myocardial hypertrophy and heart failure.