Salvianolic Acid B Prevents Iodinated Contrast Media-Induced Acute Renal Injury in Rats via the PI3K/Akt/Nrf2 Pathway

• Published in: Oxidative medicine and cellular longevity 2016-01, Vol.2016 (2016), p.1-11
• Main Authors: Ding, Xiao-qiang, Jiachang, Hu, Xialian, Xu, Nana, Song, Yu, Xiao-fang, Shaopeng, Liu, Liu, Tong-qiang, Ting, Zhang
• Format: Article
• Language: English
• Subjects: Acute Kidney Injury - chemically induced; Acute Kidney Injury - enzymology; Acute Kidney Injury - pathology; Acute Kidney Injury - prevention & control; Animals; Antioxidants; Antioxidants - pharmacology; Apoptosis; Apoptosis - drug effects; Benzofurans - pharmacology; Biomarkers - blood; Cell Line, Tumor; Chinese medicine; Comparative analysis; Contrast agents; Contrast Media; Creatinine - blood; Cytoprotection; Disease Models, Animal; Enzymes; Hospitalization; Iohexol; Kidney Tubules, Proximal - drug effects; Kidney Tubules, Proximal - enzymology; Kidney Tubules, Proximal - pathology; Kidneys; Male; Nephrology; NF-E2-Related Factor 2 - genetics; NF-E2-Related Factor 2 - metabolism; Oxidative stress; Pathogenesis; Phosphatidylinositol 3-Kinase - antagonists & inhibitors; Phosphatidylinositol 3-Kinase - metabolism; Protein Kinase Inhibitors - pharmacology; Proto-Oncogene Proteins c-akt - metabolism; Rats, Sprague-Dawley; RNA Interference; Rodents; Signal Transduction - drug effects; Transfection
• ISSN: 1942-0900; 1942-0994
• DOI: 10.1155/2016/7079487

Contrast-induced acute renal injury (CI-AKI) has become a common cause of hospital-acquired renal failure. However, the development of prophylaxis strategies and approved therapies for CI-AKI is limited. Salvianolic acid B (SB) can treat cardiovascular-related diseases. The aim of the present study was to assess the effect of SB on prevention of CI-AKI and explore its underlying mechanisms. We examined its effectiveness of preventing renal injury in a novel CI-AKI rat model. Compared with saline, intravenous SB pretreatment significantly attenuated elevations in serum creatinine and the histological changes of renal tubular injuries, reduced the number of apoptosis-positive tubular cells, activated Nrf2, and lowered the levels of renal oxidative stress induced by iodinated contrast media. The above renoprotection of SB was abolished by the PI3K inhibitor (wortmannin). In HK-2 cells, SB activated Nrf2 and decreased the levels of oxidative stress induced by hydrogen peroxide and subsequently improved cell viability. The above cytoprotection of SB was blocked by the PI3K inhibitor (wortmannin) or siNrf2. Thus, our results demonstrate that, due to its antioxidant properties, SB has the potential to effectively prevent CI-AKI via the PI3K/Akt/Nrf2 pathway.