Inhibitory effect of Ginkgo biloba extract on vascular calcification in rats with chronic kidney disease by ROS-NF-κB signaling pathway

Abstract

In order to explore the mechanism of Extract Gingko biloba (EGb761) inhibiting vascular calcification in rats with chronic kidney disease (CKD) through ROS-NF-κB signaling pathway, adult male healthy SD (Sprague Dawley) rats were selected as the research objects. Animal models were constructed and randomly divided into control group, high phosphorus-induced residual renal vascular calcification model group (HPIAC group), and EGb761 intervention calcification group. Samples were collected from each group of rats, and the renal function, aortic calcification, and the expression of related proteins were detected by Western blot. The results showed that the contents of urea nitrogen, creatinine, and phosphorus in calcification model group increased significantly, with significant statistical difference (P < 0.05), but did not decrease significantly after intervention with EGb761. In the comparative analysis of calcium content in aorta of rats in each group, it was found that the calcium content of abdominal aorta in model group was significantly higher than that in control group. After the intervention of EGb761, the calcium content of abdominal aorta was significantly decreased, with significant statistical difference (P < 0.05). Western blot was used to detect the expression levels of NF-κB (nuclear factor-κB) P65, cbfα1 (core binding factor-α1), and α-SM (a-smooth muscle) actin in thoracic aorta of rats in each group. It was found that the expression levels of NF-κB p65 and cbfα1 in thoracic aorta of rats in HPIAC group increased significantly, while the expression of α-SM actin decreased significantly, with significant statistical difference (P < 0.05). After the intervention of EGb761, the change of the protein was alleviated obviously, with significant statistical difference (P < 0.05). Therefore, through this study, it was found that EGb761 can partially alleviate the calcification of chronic renal failure (CRF) caused by high phosphorus by interfering with the expression of NF-κB p65 protein in rat thoracic artery. Although there are some shortcomings in the experiment, it still provides experimental basis for the treatment of CRF in the later clinical stage.