Ginsenoside Rb1 Treatment Attenuates Pulmonary Inflammatory Cytokine Release and Tissue Injury following Intestinal Ischemia Reperfusion Injury in Mice

Oxid Med Cell Longev. 2015:2015:843721. doi: 10.1155/2015/843721. Epub 2015 Jun 16.

Abstract

Objective. Intestinal ischemia reperfusion (II/R) injury plays a critical role in remote organ dysfunction, such as lung injury, which is associated with nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. In the present study, we tested whether ginsenoside Rb1 attenuated II/R induced lung injury by Nrf2/HO-1 pathway. Methods. II/R injury was induced in male C57BL/6J mice by 45 min of superior mesenteric artery (SMA) occlusion followed by 2 hours of reperfusion. Ginsenoside Rb1 was administrated prior to reperfusion with or without ATRA (all-transretinoic acid, the inhibitor of Nrf2/ARE signaling pathway) administration before II/R. Results. II/R induced lung histological injury, which is accompanied with increased levels of malondialdehyde (MDA), interleukin- (IL-) 6, and tumor necrosis factor- (TNF-) α but decreased levels of superoxide dismutase (SOD) and IL-10 in the lung tissues. Ginsenoside Rb1 reduced lung histological injury and the levels of TNF-α and MDA, as well as wet/dry weight ratio. Interestingly, the increased Nrf2 and HO-1 expression induced by II/R in the lung tissues was promoted by ginsenoside Rb1 treatment. All these changes could be inhibited or prevented by ATRA. Conclusion. Ginsenoside Rb1 is capable of ameliorating II/R induced lung injuries by activating Nrf2/HO-1 pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Ginsenosides / pharmacology*
  • Heme Oxygenase-1 / metabolism
  • Interleukin-10 / metabolism
  • Interleukin-6 / metabolism
  • Intestines / pathology*
  • Lung / metabolism
  • Lung / pathology
  • Male
  • Malondialdehyde / metabolism
  • Mice
  • Mice, Inbred C57BL
  • NF-E2-Related Factor 2 / antagonists & inhibitors
  • NF-E2-Related Factor 2 / metabolism
  • Reperfusion Injury / metabolism
  • Reperfusion Injury / pathology*
  • Signal Transduction / drug effects
  • Superoxide Dismutase / metabolism
  • Tretinoin / pharmacology
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Ginsenosides
  • Interleukin-6
  • NF-E2-Related Factor 2
  • Tumor Necrosis Factor-alpha
  • Interleukin-10
  • Malondialdehyde
  • Tretinoin
  • ginsenoside Rb1
  • Heme Oxygenase-1
  • Superoxide Dismutase