Baicalein Protects Rats with Diabetic Cardiomyopathy Against Oxidative Stress and Inflammation Injury Via Phosphatidylinositol 3-Kinase (PI3K)/AKT Pathway

BACKGROUND The aim of this study was to explore the effect of baicalein on diabetic cardiomyopathy (DCM) rats and the mechanisms involved, and to determine the theoretical basis for clinical anti-tumor therapy. MATERIAL AND METHODS DCM rat model was induced with a single injection of streptozotocin. Then, DCM rats were treated with baicalein alone or co-treated with baicalein and PI3K/Akt inhibitor. Myocardial pathological changes were detected by HE and Masson staining. The activities of SOD, GSH-Px, and MDA in myocardial tissue were measured by biochemical tests. The levels of TNF-α, IL-1β, and cTn-I were examined by ELISA. NADP+/NADPH ratio was measured with the NADP+/NADPH assay kit. RT-PCR was used to detect the levels of PI3K and Akt. The levels of Bax, Bcl-2, Caspase-3, GSK-3β, PI3K, and Akt were detected by Western blot. RESULTS Baicalein could improve pathological injury. SOD and GSH-Px activity decreased while the level of MDA increased in myocardial tissue. Baicalein treatment enhanced SOD activity in a dose-dependent manner but markedly reduced MDA. Similar changes were observed in both serum inflammatory factors and the NADP+/NADPH ratio. After adding PI3K-Akt inhibitor, the levels of PI3K and Akt mRNA expression were significantly decreased, but were not significantly different from the DCM group. Levels of Bcl-2, PI3K, p-GSK-3β/GSK-3β, and p-Akt were decreased in the DCM group, while the levels of Bax and Caspase-3 were obviously increased. CONCLUSIONS Baicalein can protect DCM rats against damage from oxidative stress and inflammation in myocardial tissue, and PI3K/Akt signaling pathway may be involved to mediating these effects.