Wang Lei, Liu Xiu-Heng, Chen Hui, Chen Zhi-Yuan, Weng Xiao-Dong, Qiu Tao, Liu Lin
Department of Urology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
Exp Ther Med. 2015 Apr;9(4):1253-1258. doi: 10.3892/etm.2015.2225. Epub 2015 Jan 28.
Picroside II possesses a wide range of pharmacological effects and has been demonstrated to ameliorate cerebral ischemia and reperfusion (I/R) injury. However, its effects on renal I/R injury remain unclear. In the present study, the role of picroside II in attenuating oxidative stress and the inflammatory response in a rat model of renal I/R injury was investigated. Sprague Dawley rats were subjected to 45 min of ischemia followed by 24 h of reperfusion. Prior to reperfusion, the rats were treated with picroside II or an equal volume of phosphate-buffered saline. Renal function and histological changes were compared and the relevant parameters of oxidative stress and inflammation were detected. The expression of toll-like receptor 4 (TLR4) and nuclear factor κB (NF-κB; p65) were assessed by immunohistochemistry and western blotting. It was observed that renal function was significantly improved by treatment with picroside II. Morphological analysis indicated that picroside II clearly reduced tissue damage and the expression of TLR4 and NF-κB. Reverse transcription-quantitative polymerase chain reaction demonstrated that picroside II inhibited the increase of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and intercellular adhesion molecule (ICAM)-1 expression induced by I/R injury. Western blot analysis indicated that the expression levels of TLR4 and NF-κB were significantly downregulated in the picroside II group compared with those in the I/R group. These results indicate that picroside II treatment suppressed the TLR4/NF-κB signaling pathway, protecting renal tissue against I/R-induced oxidative stress and inflammatory response.
胡黄连苷II具有广泛的药理作用，已被证明可改善脑缺血再灌注（I/R）损伤。然而，其对肾I/R损伤的影响仍不清楚。在本研究中，研究了胡黄连苷II在减轻肾I/R损伤大鼠模型中的氧化应激和炎症反应中的作用。将Sprague Dawley大鼠进行45分钟的缺血，然后再灌注24小时。在再灌注前，用胡黄连苷II或等体积的磷酸盐缓冲盐水处理大鼠。比较肾功能和组织学变化，并检测氧化应激和炎症的相关参数。通过免疫组织化学和蛋白质印迹法评估Toll样受体4（TLR4）和核因子κB（NF-κB；p65）的表达。观察到用胡黄连苷II治疗可显著改善肾功能。形态学分析表明，胡黄连苷II明显减少了组织损伤以及TLR4和NF-κB的表达。逆转录-定量聚合酶链反应表明，胡黄连苷II抑制了I/R损伤诱导的肿瘤坏死因子（TNF）-α、白细胞介素（IL）-1β和细胞间黏附分子（ICAM）-1表达的增加。蛋白质印迹分析表明与I/R组相比，胡黄连苷II组中TLR4和NF-κB的表达水平显著下调。这些结果表明，胡黄连苷II治疗抑制了TLR4/NF-κB信号通路，保护肾组织免受I/R诱导的氧化应激和炎症反应。
