Protective Effects of Polydatin on Septic Lung Injury in Mice via Upregulation of HO-1

Abstract EN

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.