Skip Navigation LinksHome > September 2010 - Volume 34 - Issue 3 > NOTOGINSENOSIDE R1 ATTENUATES RENAL ISCHEMIA-REPERFUSION INJ...
doi: 10.1097/SHK.0b013e3181ceede4
Basic Science Aspects


Liu, Wen-Jun*†; Tang, Hong-Tai*; Jia, Yi-Tao*; Ma, Bing*; Fu, Jin-Feng; Wang, Yu*; Lv, Kai-Yang*; Xia, Zhao-Fan*

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Ischemia-reperfusion (I/R) injury of the kidney is a complex pathophysiological process and a major cause of acute renal failure. It has been shown that I/R injury is related to inflammatory responses and activation of apoptotic pathways. Inhibition of certain elements of inflammatory responses and apoptotic pathway seemed to ameliorate renal I/R injury. As an effective element of Panax notoginseng, NR1 has antioxidant, anti-inflammatory, antiapoptotic, and immune-stimulatory activities. Therefore, we speculate that NR1 can attenuate renal I/R injury. Ischemia-reperfusion injury was induced by renal pedicle ligation followed by reperfusion along with a contralateral nephrectomy. Male Sprague-Dawley rats were randomized to four groups: sham group, I/R control group, NR1-1 group (rats treated with NR1, 20 mg·kg−1·d−1) and NR1-2 group (rats treated with NR1, 40 mg·kg−1·d−1). All animals were killed 72 h after I/R induction. Blood and renal tissues were collected. Renal dysfunction was observed by the level of serum creatinine and histological evaluation. Apoptosis and inflammatory response in the tissue of kidney were detected mainly with molecular biological methods. NR1 attenuated I/R-induced renal dysfunction as indicated by the level of serum creatinine and histological evaluation. It prevented the I/R-induced increases in the levels of proinflammatory cytokine TNF-α, myeloperoxidase activity, phosphorylation of p38, and activation of nuclear factor κB with cell apoptosis in the kidney and enhanced expression of antiapoptosis cytokine bcl-2. Treatment with NR1 improves renal function after I/R associated with a significant reduction in cell apoptosis and inflammatory responses, which may be related to p38 and nuclear factor κB inhibition.

©2010The Shock Society

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