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

Abstract

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.

Salvianolic acid B inhibits myofibroblast transdifferentiation in experimental pulmonary fibrosis via the up-regulation of Nrf2

“…Salvianolic acid B has been found to be anti-inflammatory, antioxidative and anti-fibrotic, especially in experimental models of renal and liver fibrosis [7,8]. Previous research has demonstrated that SalB attenuated CCl 4 -induced hepatic fibrosis [9] and inhibited TGF-b1 activation of hepatic stellate cells [10].…”

Salvianolic Acid B (Sal B) Protects Retinal Pigment Epithelial Cells from Oxidative Stress-Induced Cell Death by Activating Glutaredoxin 1 (Grx1)

“…Our data are consistent with earlier reports demonstrating that Sal B can activate Nrf2 pathway in several other organ systems. Among them, the liver [34,35], lung [36], brain [37], kidney [38], and vascular endothelial cells [19] have all been shown to be protected by Sal B pretreatment via up-regulating Nrf2 and its downstream phase II detoxification genes. Our data and these reports all indicated that Sal B can act as a potent activator of Nrf2 both in vitro and in vivo.…”

Cerebroprotection by salvianolic acid B after experimental subarachnoid hemorrhage occurs via Nrf2- and SIRT1-dependent pathways

“…Of course, in addition to HO-1, other antioxidant enzymes are also critical for maintaining cellular redox homeostasis against oxidative insults. Intriguingly, SalB was shown to induce activation of the Nrf2 signaling pathway in a variety of disease models [15,26,27]. Additionally, SalB is a potent activator of sirtuin 1 (SIRT1) [12,28,29], a nicotinamide adenine dinucleotide-dependent deacetylase implicated in a wide range of cellular functions.…”