Tanshinone IIA Attenuates Contrast-Induced Nephropathy via Nrf2 Activation in Rats

Abstract

Background/Aims: Tanshinone IIA is a chemical compound extracted from Salvia miltiorrhiza Bunge, a perennial plant also known as red sage used in traditional Chinese medicine. Tanshinone IIA has been shown to protect against various organ injuries. In this study, we hypothesized that Tanshinone IIA could play an anti-oxidative role in contrast-induced nephropathy (CIN) through enhancing Nrf2/ARE activation. Methods: To test whether Tanshinone IIA can attenuate CIN, oxidative stress, and apoptosis, we utilized two models: an in vivo Sprague-Dawley rat model of ioversol-induced CIN and an in vitro cell model of oxidative stress in which HK2 cells, a human renal tubular cell line, are treated with hydrogen peroxide (H₂O₂). Rats were randomly assigned to 4 groups (n = 6 per group): control group, ioversol group (ioversol-induced CIN), vehicle group (ioversol-induced CIN rats pretreated with vehicle), and Tanshinone IIA group (ioversol-induced CIN rats pretreated with 25mg/kg Tanshinone IIA). Renal functions, renal injuries and apoptosis were evaluated by using serum creatinine, histological scoring, and TUNEL staning respectively. Malondialdehyde, 8-hydroxy-2’ –deoxyguanosine, and intracellular reactive oxygen species were used for oxidative stress assessment. Levels of Nrf2 and heme oxygenase-1 (HO-1) were measured in vivo and in vitro. Results: Tanshinone IIA attenuated renal tubular necrosis, apoptosis and oxidative stress in rats and oxidative stress in HK2 cells. Furthermore, Tanshinone IIA activated Nrf2, and up-regulated HO-1 expression in vivo and in vitro, resulting in a reduction in oxidative stress. Conclusion: Tanshinone IIA may protect against CIN through enhancing Nrf2/ARE activation.

tert-Butylhydroquinone Treatment Alleviates Contrast-Induced Nephropathy in Rats by Activating the Nrf2/Sirt3/SOD2 Signaling Pathway

“…The levels of BUN and SCR were higher in the ioversol-treated group than in the control group. Significantly, similar results were obtained in vitro using HK-2 cells and were consistent with a previously published study [25]. Like the earlier report, our study also showed that pretreatment with t-BHQ, an agonist of Nrf2, could mitigate oxidative stress and alleviate the progression of AKI.…”

“…Nrf2 is an important transcription factor belonging to the E26 transformation-specific (ETS) factor family that regulates the cellular resistance to oxidants, including radiocontrast agents [26]. Previous studies have shown that Nrf2 plays a renoprotective role in CIN [25,27]. Sirt3, which is an NAD + -dependent deacetylase localized in the mitochondrial matrix, regulates a variety of cellular processes, including oxidative stress, ATP generation, and energy metabolism.…”

RETRACTED: Tanshinone I attenuates the malignant biological properties of ovarian cancer by inducing apoptosis and autophagy via the inactivation of PI3K/AKT/mTOR pathway

“…[7][8][9][10] The tanshinones consist of four major constituents, such as tanshinone Ⅰ (Tan-Ⅰ), tanshinone IIA, crytotanshinone and dihydrotanshinone Ⅰ, and their biological effects have been a prime research focus. [11][12][13][14] The major constituents of Dan-shen have been recently shown to possess some activities against human cancer cells.…”

Adropin reduces hypoxia/reoxygenation‑induced myocardial injury via the reperfusion injury salvage kinase pathway

“…Myocardial cells generate numerous reactive oxygen species during the ischemia-reperfusion process and increase TNF-α synthesis, which can lead to an increase in the apoptosis cascade reaction, the interactions between inflammatory and endothelial cells and intracellular calcium overload (22). Various novel antioxidants have been associated with renal protection through the antioxidative and antiapoptotic pathways (23,24). A previous study (9) has demonstrated that adropin is negatively correlated with the inflammatory marker C reactive protein.…”