The effects of pentoxifylline and caffeic acid phenethyl ester on TNF-α and lung histopathology in D-galactosamine-induced pulmonary injury in rats

Tissue Cell. 2023 Jun:82:102085. doi: 10.1016/j.tice.2023.102085. Epub 2023 Apr 1.

Abstract

In this study, we aimed to investigate the effects of pentoxifylline [PTX] and caffeic acid phenethyl ester [CAPE] in D-galactosamine [D-GAL]-induced pulmonary injury in rats. The rats were randomly divided into six groups: control, D-GAL, D-GAL+PTX, D-GAL+CAPE, PTX and CAPE. Each group included eight animals. Lung sections from the control, PTX and CAPE groups had a normal histological appearance. The D-GAL group showed histopathological changes in lung tissue, including haemorrhage, oedema, inter-alveolar septal thickening and widespread infiltration of inflammatory lymphocytes and macrophages. Administration of PTX and CAPE significantly reduced histopathological damage scores in the D-GAL+PTX and D-GAL+CAPE groups compared with the D-GAL group. PTX and CAPE treatment also significantly decreased malondialdehyde levels, increased levels of reduced GSH and increased catalase and superoxide dismutase activity in lung tissue samples. These results indicate that the destructive effects of D-GAL-induced inflammation in the rat lung are significantly reduced following administration of PTX and CAPE.

Keywords: Caffeic acid phenethyl ester; Galactosamine; Lung; Pentoxifylline; Rat.

Publication types

  • Review

MeSH terms

  • Animals
  • Antioxidants / pharmacology
  • Caffeic Acids / pharmacology
  • Catalase
  • Galactosamine / toxicity
  • Lung / pathology
  • Lung Injury* / chemically induced
  • Lung Injury* / drug therapy
  • Lung Injury* / pathology
  • Malondialdehyde
  • Pentoxifylline* / pharmacology
  • Rats
  • Superoxide Dismutase
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Pentoxifylline
  • caffeic acid phenethyl ester
  • Tumor Necrosis Factor-alpha
  • Superoxide Dismutase
  • Galactosamine
  • Catalase
  • Caffeic Acids
  • Malondialdehyde
  • Antioxidants