The novel effects of Aspalathus linearis (Rooibos) against angiotensin-II-induced hypertrophy in H9C2 cardiomyoblasts

• Angiotensin-II induced hypertrophy and apoptosis in H9C2 cardiomyoblasts. • Rooibos protected against Angiotensin-II-induced hypertrophy and apoptosis. • Rooibos enhanced antioxidant activity, specifically superoxide dismutase activity. • Rooibos presented protective effects by improving hypertrophic signalling markers. Cardiovascular disease (CVD) remains the leading cause of death worldwide. Elevated oxidative stress and hypertrophy play a crucial role in the pathogenesis of CVD. These key features are interconnected, whereby oxidative stress drives cardiac hypertrophy, which subsequently enhances apoptosis and exacerbates myocardial damage. Existing treatments present several limitations, including adverse effects, highlighting the need for improved therapeutic interventions. Aspalathus linearis , commonly known as Rooibos (RB), has demonstrated antioxidant properties. Emerging evidence suggests that RB may reduce CVD risk, but there is a lack of studies demonstrating the anti-hypertrophic actions of RB in a cardiac context. Additionally, the underlying molecular mechanisms require further investigation. Therefore, this study aimed to investigate the effects of RB in an H9C2 cardiomyoblast model of Ang-II-induced hypertrophy. H9C2 cardiomyoblasts were cultured and treated for 48 h as follows: Ang-II (20 μM), RB extract (100 μg/ml), Ang-II+RB and Ang-II+Losartan (Los) (10 μM). Post-treatment, cell size and cell viability were assessed. Antioxidant activity, particularly superoxide dismutase (SOD) and catalase (CAT) activity were evaluated, and lipid peroxidation was assessed. Additionally, levels of hypertrophic signalling proteins were examined. Ang-II increased cell size, reduced cell viability, increased MDA levels, enhanced the inhibition of GSK3β, reduced total ERK1/2, and reduced mTOR. In turn, co-treatment with RB protected against these effects as we observed reduced cell size and increased cell viability, increased SOD activity, increased total NFAT1, a reduction in the inhibition of GSK3β, increased total ERK2, and an increase in mTOR levels. These findings highlight the protective potential of RB in the context of cardiomyoblast hypertrophy, further supporting its cardioprotective properties.