Ligustrazine attenuates acute lung injury induced by blunt chest trauma

Saudi Med J. 2012 Feb;33(2):139-45.

Abstract

Objective: To investigate the effects of ligustrazine on acute lung injury induced by blunt chest trauma.

Methods: This study was performed in the Animal Center of Renmin Hospital of Wuhan University, Wuhan, China between September 2009 and September 2010. Male Sprague-Dawley rats were randomly allocated into 4 groups: sham control group (group C, n=60), ligustrazine treatment group (group C+L, n=60), blunt chest trauma model group (group T, n=60), and the trauma plus ligustrazine treatment group (group T+L, n=60). The lung contusion was induced as previously described. Animals of the T+L group were intraperitoneally injected with ligustrazine. Acute lung injury was evaluated by histopathology of the lung, and apoptosis was determined by terminal dUTP nick-labeling. Pulmonary edema was estimated using Evans blue dye extravasation and wet/dry ratios of lung tissue. The expression of caspase-3, Bcl-2, and Bax in the lung, as well as blood plasma tumor necrosis factor (TNF)-alpha were also measured.

Results: The ligustrazine treatment significantly attenuated lung injury induced by blunt chest trauma, as shown by decreased apoptosis index, and pulmonary edema (p=0.04). The blood plasma TNF-alpha level after blunt chest trauma significantly deceased after the administration of ligustrazine (p=0.03). In addition, the ligustrazine treatment significantly alleviated the expression of caspase-3 (p=0.03), and increased the ratio of Bcl-2 to Bax (p<0.03).

Conclusion: Ligustrazine effectively protects lung injury induced by blunt chest trauma, and the protective effects seem to be mediated by attenuation of cell apoptosis via an increased ratio of Bcl-2/Bax and decreased caspase-3 activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Lung Injury / drug therapy*
  • Acute Lung Injury / metabolism
  • Acute Lung Injury / pathology
  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
  • Apoptosis / drug effects
  • Caspase 3 / drug effects
  • Caspase 3 / metabolism
  • Male
  • Proto-Oncogene Proteins c-bcl-2 / drug effects
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Pulmonary Edema / metabolism
  • Pyrazines / pharmacology*
  • Pyrazines / therapeutic use
  • Rats
  • Rats, Sprague-Dawley
  • Thoracic Injuries / drug therapy*
  • Thoracic Injuries / metabolism
  • Thoracic Injuries / pathology
  • Tumor Necrosis Factor-alpha / blood
  • Tumor Necrosis Factor-alpha / drug effects
  • Wounds, Nonpenetrating / drug therapy*
  • Wounds, Nonpenetrating / metabolism
  • Wounds, Nonpenetrating / pathology
  • bcl-2-Associated X Protein / drug effects
  • bcl-2-Associated X Protein / metabolism

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Proto-Oncogene Proteins c-bcl-2
  • Pyrazines
  • Tumor Necrosis Factor-alpha
  • bcl-2-Associated X Protein
  • Caspase 3
  • tetramethylpyrazine