In order to explore the mechanism of Extract Gingko biloba (EGb761) inhibiting vascular calcification in rats with chronic kidney disease (CKD) through ROS-NF-kappa B 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-kappa B (nuclear factor-kappa B) P65, cbf alpha 1 (core binding factor-alpha 1), and alpha-SM (a-smooth muscle) actin in thoracic aorta of rats in each group. It was found that the expression levels of NF-kappa B p65 and cbf alpha 1 in thoracic aorta of rats in HPIAC group increased significantly, while the expression of alpha-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-kappa B 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. (C) 2019 The Author(s). Published by Elsevier B.V. on behalf of King Saud University.

Objective: We sought to investigate the effect of variations in pH on vascular calcification (VC) in rats with chronic kidney disease (CKD) and the expression of Runt-related transcription factor 2. Methods: A total of healthy male Sprague-Dawley rats of a clean grade were randomly stratified into a control group, CKD group, CKD with VC (CKD+VC) group, acid intervention (CKD+VC+AC) group, and alkaline intervention (CKD+VC+AC) group. Rat models with CKD, chronic metabolic acidosis, and chronic metabolic alkalosis were established. Rat arterial pH values and HCO3- concentrations were detected by blood gas analysis. Serum creatinine (SCR) and urea nitrogen (BUN) content were detected by automatic biochemical analysis. Calcium content was determined by o-cresol oxime complex ketone colourimetry. The calcification condition of rat thoracic aorta and Runt-related transcription factor 2 expression were detected by Von Kossa staining and immunohistochemistry, respectively. Results: The levels of SCR and BUN were much higher in the CKD group, CKD+VC group, CKD+VC+AC group, and CKD+VC+BC group than in the control group (P<0.05). Separately, pH level and HCO3- concentration results were much lower in the CKD+VC+AC group than in the CKD+VC group (P<0.05) but were much higher in the CKD+VC+BC group than in the CKD+VC group (P<0.05). Also, the calcium contents of the thoracic aorta were significantly higher in the CKD+VC and CKD+VC+BC groups than in the control group, much lower in the CKD+VC+AC group than in the control group, and much higher in the CKD+VC+BC group than in the control group. (P<0.05). There were many brown-black calcium deposits noted in the media layer of the thoracic aorta of rats in the CKD+VC group and CKD+VC+BC group (P<0.05), while no such findings were observed in the control group, CKD group, or CKD+VC+AC group (P<0.05); further, the level of brown-black calcium deposition in the media layer of the thoracic aorta was much higher in the CKD+VC+BC group than in the CKD+VC group (P<0.05). Finally, the CKD+VC group and CKD+VC+BC group had significantly higher RUNX2 immunohistochemical scores than did the control group or CKD group (P<0.05), while the RUNX2 immunohistochemical scores were much lower in the CKD+VC+BC but much higher in the CKD+VC+BC group than in the CKDD+VC group (P<0.05). Conclusions: An acidic pH environment inhibits the occurrence of VC in rats with CHD and an alkaline environment promotes VC in rats with the same, which may be achieved by regulating RUNX2 expression.