Rosmarinic acid from Mentha arvensis attenuates Angiotensin II-induced cell death, cellular senescence, and mitochondrial depolarization in Human Umbilical Vein Endothelial cells

Endothelial dysfunction plays a pivotal role in the progression of cardiovascular diseases and vascular complications associated with diabetes mellitus. Considering the significant mitigating effects that phytochemicals can have on endothelial dysfunction, further research in this area is warranted, forming the basis of this study. This research aims to evaluate the impact of rosmarinic acid (RA), a phenolic compound isolated from Mentha arvensis, on experimental endothelial dysfunction induced by Angiotensin II (Ang II). The purity of the compound was verified through HPLC analysis, and Human Umbilical Vein Endothelial Cells (HUVECs) were utilized as the in vitro model for the investigations. Cytotoxicity of RA was assessed at various concentrations to determine the optimal concentration. RA demonstrated remarkable efficacy in preventing cell death induced by Ang II, increasing viability to 92% after it had been reduced to 53% by Ang II alone. Co-treatment with RA also reduced membrane injury, as evidenced by the LDH leakage assay. The ability of RA to mitigate cellular senescence induced by Ang II was assessed using the X-gal staining method. Analysis of mitochondrial membrane potential through TMRE flow cytometry revealed that groups co-treated with RA exhibited reduced mitochondrial depolarization compared to the Ang II group. This research confirms the protective effect of RA against both cellular and mitochondrial dysfunction induced by Ang II in HUVECs