Ding Xiao-qiang

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

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.

Epidemiology and Management of Acute Kidney Injury in Hepatocellular Carcinoma Patients Undergoing Transcatheter Arterial Chemoembolization

Transcatheter arterial chemoembolization (TACE) is an effective therapy for hepatocellular carcinoma (HCC). However, acute kidney injury (AKI) may occur after TACE due to the contrast agent and cytotoxic anticancer drugs used in this procedure. Post-TACE AKI is not an unusual event, and may adversely affect patient outcome. Coexisting situations including cirrhosis, renal insufficiency, diabetes and hypertension play a role in the development of HCC, and may predispose patients to AKI after TACE. Most post-TACE are transient and reversible, while prolonged AKI may predict a decreased survival. The best strategy to manage post-TACE AKI is prevention. Patients, before undergoing TACE, should be carefully assessed. In this study, we reviewed the current literature published in English about the incidence rate, risk factors, management and prognosis of AKI in patients with HCC undergoing TACE for a better understanding of this complication.

Effect of Body Mass Index on Acute Kidney Injury After Cardiac Surgery

Background: Trichorhinophalangeal 1 (Trps1) is essential for epithelial cell morphogenesis during kidney development. But its role in acute kidney injury induced by ischemia/reperfusion (I/R) remains unclear. Methods: The rat models of renal I/R injury were established by clamping bilateral renal arteries for 45 min (moderate I/R) or for 60 min (severe I/ R) and reperfusion. The renal tubule epithelial NRK-52E cells were cultured under hypoxic conditions for 4 h to induce hypoxic injury, followed by reoxygenation (H/R). Trps1-siRNA or Trps1-overexpression vectors were transferred by ultrasound-microbubble-mediated gene transfer system. The changes of gene expression were analyzed by real-time PCR and Western blotting. Promoter activities of transcription factors were estimated by dual luciferase reporter gene assay. Results: Knockdown of Trps1 significantly delayed renal repair in moderate I/R model as evidenced by higher serum creatinine levels and more severe morphological injury compared with wild-type rat (P < 0.05), whereas overexpression of Trps1 significantly accelerated renal repair after severe I/R injury. Knockdown of Trps1 decreased the proportion of IdU positive cells in rat kidneys with I/R injury and the level of PCNA in NRK-52E cells after H/R, and vice versa. Furthermore, mRNA level of Notch2 was decreased by 58% and the protein levels of Notch2 and its downstream effector molecule Hes1 were decreased by about 43e67% in Trps1-knockdown rat at 3 day after reperfusion. The dual luciferase analysis demonstrated that Trps1 directly activated Notch2 transcription. And knockdown of Notch2 significantly inhibited Trps1-induced tubular cells proliferation in vitro. Conclusion: Trps1 regulates tubular cells proliferation through Notch2 and promotes kidney repair after I/R injury. Trps1 may serve as a potential therapeutic target for renal repair following I/R injury.