Heme Oxygenase-1 Expresion in Gastric Mucosa and Liver after Burns: Preliminary Immunohistochemical Study

Abstract

Ganka Bekyarova , Maria Tzaneva , Minka Hristova

Objective: Generation of reactive oxygen metabolites (ROM) and oxidative stress are crucial in pathogenesis of thermal skin injury. Heat shock proteins such as HSP32 known as heme oxygenase-1 (HO-1) possesses antioxidant, anti-inflammatory, and vasodilative properties and play an important role in the protecting of tissues from several stresses. In this immunohistochemical study, we have assessed the constitutive expression of HO-1 in normal gastric mucosa and liver and tested the hypothesis that its expression in these tissues is upregulated in thermal skin injury characterized by increased production of ROMs and other pro-inflammatory mediators. We used malondialdehyde (MDA) as a marker of oxidative stress and tumor necrosis factor-alpha (TNF-α) as a marker of inflammatory response in burn rat model. Methods: HO-1 expression in formalin-fixed sections was assessed by peroxidase antiperoxidase immunohistochemistry using a polyclonal rabbit anti-HO-1 as primary antibody. TNF-α in plasma was quantified using enzyme-linked immunosorbent assay (ELISA) kit. Spectrometric method was used for plasma and tissue MDA assay. Results: Immunohistochemical staining revealed HO-1 expression in all groups. Staining scores for HO-1 in endothelial cells in both gastric mucosa and liver were increased with 32% (p <0.001) and 51 % (p< 0.001), compared to that of controls. The levels of MDA in the gastric mucosa were increased by 43% (p<0.05) and in liver in 126% (p<0.001). Plasma concentration of TNF-α was also elevated by 111 % (p<0.001) and MDA level in plasma was increased by 37% (p<0.05). Conclusion: Our data suggest that HO-1 induction following burn is an adaptive response which can protect gastric mucosal and liver against further oxidative damage. HO-1 system may represent a target and an effective and cooperative strategy to intervene in the protection against inflammatory processes and oxidative tissue injury.