Ginkgetin aglycone attenuates the apoptosis and inflammation response through nuclear factor-kB signaling pathway in ischemic-reperfusion injury.

Abstract

Acute myocardial infarction (AMI) is one of the most threaten disease in the world. Ginkgetin aglycone (GA) was a new kind of Ginkgo biloba, involved in various diseases, including kidney injury and acute pancreatitis. However, the function of GA in AMI remains unknown. The aim of the study was to investigate the characteristics and function of GA in ischemic-reperfusion injury. H2 O 2 - and CoCl 2 -treated H9C2 cells were used to analyze the function of GA in vitro. Caspase 3, interleukin-6 (IL-6), and tumor necrosis factor-α were detected to evaluate the apoptosis and inflammation response. Rat AMI was performed to elucidate the function in vivo. We found that GA could reduce the apoptosis and improved cell survival of H2 O 2 -treated H9C2 cardiomyocytes and CoCl 2 -treated H9C2 cells. GA attenuated CoCl 2 -induced inflammatory response and the level of cleaved caspase 33, suggesting that GA could alleviate the cell apoptosis. GA improved the cardiac function and attenuated the inflammatory cell infiltration in vivo. We also found that nuclear factor-kB signaling pathway, which was activated under hypoxia environment, was also suppressed in the GA-treated group. We verified the function and mechanism of GA and provide evidence that GA may play a vital role in ischemic-reperfusion injury, and understanding the precise role of GA will undoubtedly shed new light on the clinical treatment.