Astaxanthin Protects Against Diabetic Cardiomyopathy Via Activation of Akt Pathway in H9c2 Cells

Purpose: To investigate the cardioprotective action of astaxanthin, and to elucidate its underlying mechanism of action in H9c2 cells. Methods: Cell viability was determined by MTT assay. Intracellular reactive oxygen species (ROS) were evaluated using 2, 7-dichlorodihydro-fluorescein diacetate (H2DCFDA) staining. Cell apoptosis were assessed by determining caspase activities using colorimetric assay. The apoptotic cells were labelled with annexin V/PI staining and quantified by flow cytometry. Involvement of Akt signaling pathway was verified using western blot. Results: The results revealed that astaxanthin (5 and 10 pM) dose-dependently reversed high glucose-induced cell viability loss in H9c2 cells (p < 0.01 and p < 0.001, respectively). Astaxanthin inhibited intracellular ROS production, decreased caspase 3 and caspase 9 activities in high glucose-challenged H9c2 cells in a concentration-related manner (p < 0.05). Besides, astaxanthin markedly inhibited the number of apoptotic H9c2 cells induced by high glucose. Furthermore, western blot analysis demonstrated that astaxanthin upregulated the activation of Akt signaling. Conclusion: Astaxanthin may protect high glucose induced diabetic cardiomyopathy via activation of Akt pathway, and thus deserves further investigation as a cardioprotective agent.