Protective effects of polydatin on septic lung injury in mice via upregulation of HO-1.

Abstract

The present study was carried out to investigate the effects and mechanisms of polydatin (PD) in septic mice. The model of cecal ligation and puncture (CLP-)induced sepsis was employed. Pretreatment of mice with PD (15, 45, and 100 mg/kg) dose-dependently reduced sepsis-induced mortality and lung injury, as indicated by alleviated lung pathological changes and infiltration of proteins and leukocytes. In addition, PD inhibited CLP-induced serum tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) production, lung cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase isoform (iNOS) protein expressions and NF-κB activation. Notably, PD upregulated the expression and activity of heme oxygenase (HO-)1 in lung tissue of septic mice. Further, the protective effects of PD on sepsis were abrogated by ZnPP IX, a specific HO-1 inhibitor. These findings indicated that PD might be an effective antisepsis drug.

• Authors: Xiao-hui Li, Xia Gong, Li Zhang, Rong Jiang, Hong-zhong Li, Meng-jiao Wu, Jing-yuan Wan
• Journal: Mediators of inflammation (Mediators Inflamm) Vol. 2013 Pg. 354087 ( 2013) ISSN: 1466-1861 [Electronic] United States
• PMID: 23431240 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Glucosides
• Interleukin-6
• Stilbenes
• Transcription Factor RelA
• Tumor Necrosis Factor-alpha
• Nitric Oxide
• Heme Oxygenase-1
• polydatin

Topics

• Animals
• Bronchoalveolar Lavage Fluid
• Glucosides (therapeutic use)
• Heme Oxygenase-1 (metabolism)
• Interleukin-6 (blood)
• Lung Injury (blood, drug therapy, enzymology)
• Mice
• Nitric Oxide (metabolism)
• Random Allocation
• Sepsis (blood, enzymology, metabolism)
• Stilbenes (therapeutic use)
• Transcription Factor RelA (metabolism)
• Tumor Necrosis Factor-alpha (blood)