Fu Haiyan, Hu Zhansheng, Di Xingwei, Zhang Qiuhong, Zhou Rongbin, Du Hongyang
Intensive Care Unit in the first affiliated hospital of Jinzhou Medical University, Jinzhou, 121000 Liaoning, China; Department of Dermatology, Beijing Children's Hospital, Capital Medical University, Beijing, 100045, China.
Intensive Care Unit in the first affiliated hospital of Jinzhou Medical University, Jinzhou, 121000 Liaoning, China.
Eur J Pharmacol. 2016 Nov 15;791:229-234. doi: 10.1016/j.ejphar.2016.08.013. Epub 2016 Aug 18.
Tenuigenin (TNG) has been reported to have various pharmacological activities, such as anti-oxidative and anti-inflammatory activities. However, the protective effects of TNG on lipopolysaccharides (LPS)-induced acute kidney injury (AKI) are still not clear. The aim of this study was to investigate the protective effects and mechanism of TGN on LPS-induced AKI in mice. The kidney histological change, levels of blood urea nitrogen (BUN), and creatinine were measured to assess the protective effects of TNG on LPS-induced AKI. The levels of TNF-α, IL-1β, and IL-6 in serum and kidney tissues were detected by ELISA. The extent of nuclear factor kappa-B (NF-κB) p65 and the expression of Toll-like receptor-4 (TLR4) were detected by western blot analysis. The results showed that TNG markedly attenuated the histological alterations, BUN and creatinine levels in kidney. TNG also suppressed LPS-induced TNF-α, IL-1β, and IL-6 production. Furthermore, the expression of TLR4 and NF-κB activation induced by LPS were markedly inhibited by TNG. In conclusion, this study demonstrated that TNG protected against LPS-induced AKI by inhibiting TLR4/NF-κB signaling pathway.
据报道,土贝母苷甲(TNG)具有多种药理活性,如抗氧化和抗炎活性。然而,TNG对脂多糖(LPS)诱导的急性肾损伤(AKI)的保护作用仍不清楚。本研究的目的是探讨TGN对LPS诱导的小鼠AKI的保护作用及其机制。检测肾脏组织学变化、血尿素氮(BUN)和肌酐水平,以评估TNG对LPS诱导的AKI的保护作用。通过酶联免疫吸附测定(ELISA)检测血清和肾脏组织中肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)的水平。通过蛋白质免疫印迹分析检测核因子κB(NF-κB)p65的程度和Toll样受体4(TLR4)的表达。结果表明,TNG显著减轻了肾脏的组织学改变、BUN和肌酐水平。TNG还抑制了LPS诱导的TNF-α、IL-1β和IL-6的产生。此外,TNG显著抑制了LPS诱导的TLR4表达和NF-κB激活。总之,本研究表明,TNG通过抑制TLR4/NF-κB信号通路对LPS诱导的AKI具有保护作用。