Caspase inhibitor zVAD-fmk protects against acute pancreatitis-associated lung injury via inhibiting inflammation and apoptosis

Pancreatology. 2016 Sep-Oct;16(5):733-8. doi: 10.1016/j.pan.2016.06.002. Epub 2016 Jun 6.

Abstract

Background/objectives: Pulmonary apoptosis is an important pathogenic mechanism of acute lung injury induced by many factors. This study aims to investigate whether the caspase inhibitor zVAD-fmk has a protective effect against lung injury in the severe acute pancreatitis model (SAP) in rats.

Methods: Seventy-two Sprague-Dawley rats were randomly divided into Sham, SAP, and SAP + zVAD-fmk groups. The SAP model was established by injection of 5% sodium taurocholate into the pancreatic duct. Animals were sacrificed at 3 h, 6 h, 12 h, and 24 h after operation and then HE staining analysis was performed to assess the lung injury. ELISA was used to detect the activity of myeloperoxidase (MPO) and the concentrations of tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β). Western blotting was used to detect the expression of cleaved caspase-3 in the lung tissues.

Results: Rats in SAP group showed obvious lung injury through pathologic examination. Pretreatment with zVAD-fmk significantly inhibited a post-SAP increase in the activation of MPO, TNF-α, IL-1β, and caspase-3, and decreased lung injury induced by SAP as determined by the pathologic score.

Conclusion: Our results suggest that apoptosis plays an important role in acute pancreatitis-associated lung injury (APALI), and inhibition of caspase activity may represent a new therapeutic approach for the treatment of APALI.

Keywords: Acute pancreatitis-associated lung injury; Apoptosis; Caspase; Inflammation; zVAD-fmk.

MeSH terms

  • Acute Lung Injury / etiology*
  • Acute Lung Injury / pathology
  • Acute Lung Injury / prevention & control*
  • Amino Acid Chloromethyl Ketones / therapeutic use*
  • Amylases / blood
  • Animals
  • Apoptosis / drug effects*
  • Caspase 3 / biosynthesis
  • Caspase Inhibitors / therapeutic use*
  • Inflammation / etiology*
  • Inflammation / prevention & control*
  • Interleukin-1beta / antagonists & inhibitors
  • Male
  • Pancreatic Ducts / pathology
  • Pancreatitis / chemically induced
  • Pancreatitis / complications*
  • Pancreatitis / pathology
  • Rats
  • Rats, Sprague-Dawley
  • Taurocholic Acid
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors

Substances

  • Amino Acid Chloromethyl Ketones
  • Caspase Inhibitors
  • IL1B protein, rat
  • Interleukin-1beta
  • Tumor Necrosis Factor-alpha
  • benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone
  • Taurocholic Acid
  • Amylases
  • Casp3 protein, rat
  • Caspase 3