Ginsenoside Rb1 attenuates intestinal ischemia reperfusion induced renal injury by activating Nrf2/ARE pathway.

Abstract

Intestinal ischemia reperfusion (IIR) is a serious clinical condition associated with simultaneous multiple organ dysfunction. The aim of this study was to investigate the effects of ginsenoside Rb1 on IIR induced renal injury in mice. An intestinal ischemia reperfusion mouse model was established by superior mesenteric artery (SMA) occlusion for 45 min, followed by reperfusion for 2 h. IIR induced renal injury characterized by increase of BUN, Cr and NGAL in serum, MDA levels and decrease of SOD levels in the renal tissues. Ginsenoside Rb1 (30, 60 mg/kg) given intraperitoneally before reperfusion attennuated renal injury, which was associated with decrease of BUN, Cr and NGAL in serum, MDA levels and increase of SOD levels in the renal tissues. Furthermore, the immunohistochemistry and Western blot data showed that ginsenoside Rb1 dramatically reversed IIR induced renal injury, associated with upregulated nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in renal tissues. Our data suggests that ginsenoside Rb1 attenuates acute renal injury induced by intestinal ischemia reperfusion by activating the Nrf2/ARE pathway.

• Authors: Qian Sun, Qing-Tao Meng, Ying Jiang, Zhong-Yuan Xia
• Journal: Molecules (Basel, Switzerland) (Molecules) Vol. 17 Issue 6 Pg. 7195-205 (Jun 12 2012) ISSN: 1420-3049 [Electronic] Switzerland
• PMID: 22692243 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Ginsenosides
• NF-E2-Related Factor 2
• Malondialdehyde
• ginsenoside Rb1
• Heme Oxygenase-1
• Superoxide Dismutase

Topics

• Acute Kidney Injury (etiology, metabolism, physiopathology)
• Animals
• Ginsenosides (administration & dosage, pharmacology)
• Heme Oxygenase-1 (metabolism)
• Intestines (blood supply)
• Ischemia (complications)
• Kidney (drug effects, metabolism, pathology)
• Male
• Malondialdehyde (metabolism)
• Mice
• Mice, Inbred C57BL
• NF-E2-Related Factor 2 (metabolism)
• Reperfusion Injury (complications, drug therapy)
• Signal Transduction
• Superoxide Dismutase (metabolism)