Salvianolic Acid B Prevents Iodinated Contrast Media-Induced Acute Renal Injury in Rats via the PI3K/Akt/Nrf2 Pathway.
Salvianolic Acid B Prevents Iodinated Contrast Media-Induced Acute Renal Injury in Rats via the PI3K/Akt/Nrf2 Pathway.
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丹酚酸 B 通过 PI3K/Akt/Nrf2 通路预防碘造影剂引起的大鼠急性肾损伤
DOI：
10.1155/2016/7079487
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发表时间：
2016
影响因子：
--
通讯作者：
Xiaoqiang D
中科院分区：
文献类型：
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作者：
Tongqiang L;Shaopeng L;Xiaofang Y;Nana S;Xialian X;Jiachang H;Ting Z;Xiaoqiang D
造影剂诱导的急性肾损伤（阿基）已成为医院获得性肾衰竭的常见原因。然而，阿基的预防策略和获批治疗的发展有限。丹参素B（SB）可治疗心血管相关疾病。本研究的目的是评估SB预防阿基的效果并探讨其潜在机制。我们在新型阿基大鼠模型中检查了其预防肾损伤的有效性。与生理盐水相比，静脉SB预处理显著减弱了血清肌酐升高和肾小管损伤的组织学变化，减少了凋亡阳性肾小管细胞的数量，激活了Nrf 2，并降低了碘化造影剂诱导的肾脏氧化应激水平。SB的上述肾保护作用可被PI 3 K抑制剂wortmannin所阻断。在HK-2细胞中，SB激活Nrf 2并降低过氧化氢诱导的氧化应激水平，随后提高细胞活力。SB的上述细胞保护作用可被PI 3 K抑制剂（wortmannin）或siNrf 2阻断。因此，我们的研究结果表明，由于其抗氧化特性，SB具有通过PI 3 K/Akt/Nrf 2途径有效预防阿基的潜力。
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.