Picroside II protects rat kidney against ischemia/reperfusion-induced oxidative stress and inflammation by the TLR4/NF-κB pathway

• Published in: Experimental and therapeutic medicine 2015-04, Vol.9 (4), p.1253-1258
• Main Authors: WANG, LEI, LIU, XIU-HENG, CHEN, HUI, CHEN, ZHI-YUAN, WENG, XIAO-DONG, QIU, TAO, LIU, LIN
• Format: Article
• Language: English
• Subjects: Binding sites; Bioengineering; Care and treatment; Chinese medicine; Cytokines; Inflammation; Ischemia; ischemia and reperfusion injury; Kidney diseases; Kidneys; Kinases; Laboratory animals; Oxidative stress; picroside II; Proteins; Rodents
• ISSN: 1792-0981; 1792-1015
• DOI: 10.3892/etm.2015.2225

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.