Astragaloside IV Attenuates Angiotensin II-Induced Inflammatory Responses in Endothelial Cells: Involvement of Mitochondria.

Background: Angiotensin II (Ang II)-triggered endothelial inflammation is a critical mechanism contributing to Ang II-related cardiovascular diseases. The inflammation is highly correlated with mitochondrial function. Although astragaloside IV (AS-IV), a primary bioactive ingredient extracted from the traditional Chinese medicine Methods: Human umbilical vein endothelial cells (HUVECs) were preincubated with AS-IV and then exposed to Ang II for 12 h. Results: The exposure of HUVECs to Ang II triggered cytokine and chemokine production, the upregulation of adhesive molecules, monocyte attachment, and nuclear factor-kappa B activation. Additionally, our results showed that the inflammatory responses triggered by Ang II were associated with the impairment of mitochondrial function, as evidenced by the reductions of mitochondrial membrane potential, ATP synthesis, and mitochondrial complexes I and III activities. Moreover, the concentrations of malondialdehyde, cellular reactive oxygen species, and mitochondrial superoxide enhanced after HUVECs challenged with Ang II, which were concurrent with the decreases in total superoxide dismutase (SOD) and its isoenzyme activities such as Mn-SOD. These Ang II-induced alterations were reversed by preincubation with AS-IV. Conclusion: Our data indicate that AS-IV attenuates Ang II-triggered endothelial inflammation possibly via ameliorating mitochondrial function.