Cardioprotective effects of daidzein: Exploring the role of the NRG-1/Akt pathway in a rat model of isoproterenol-induced myocardial infarction.

BACKGROUND AND AIMS: This study aimed to evaluate the cardioprotective effects of daidzein, an antioxidant and anti-inflammatory compound, focusing on its impact on the NRG-1/Akt signaling pathway in a rat model of isoproterenol (ISO)-induced myocardial infarction (MI).

METHODS AND

RESULTS

Twenty-eight male Sprague Dawley rats were divided into four groups: Control, MI, MI + DMSO, and MI + Daidzein. MI was induced with ISO (85 mg/kg) subcutaneously twice with a 24-h intervals. Daidzein was administered intraperitoneally (10 mg/kg) daily for seven days post-MI. Serum troponin were measured 24 h after MI to confirm injury. Cardiac tissues were analyzed for total antioxidant status (TAS), total oxidant status (TOS), Neuregulin-1 (NRG-1), erythroblastic leukemia viral oncogene homolog 2 (ErbB2), and Protein Kinase B (Akt) levels using ELISA. Histopathological and immunohistochemical evaluations were conducted. TOS and oxidative stablity index (OSI) levels were significantly higher in the MI group compared to the Control (P < 0.05), but daidzein treatment significantly reduced these levels (P = 0.014, P = 0.036). NRG-1 and ErbB2 levels were decreased in the MI group compared to Control (P = 0.029, P = 0.001) but restored by daidzein (P = 0.026, P = 0.01). Immunohistochemistry showed increased NRG-1 and ErbB2 in cardiac tissue following daidzein treatment, and histopathology confirmed reduced inflammation, damage, and fibrosis (P < 0.05).

CONCLUSION

Daidzein demonstrated cardioprotective effects by reducing oxidative stress and improving molecular and structural cardiac parameters post-MI, likely through activation of the NRG-1/Akt pathway. Further research is needed to explore its therapeutic potential in cardiovascular disease.