The protective effects of heat shock protein 22 in lung ischemia-reperfusion injury mice

Abstract

Lung ischemia-reperfusion injury (LIRI) often results in respiratory insufficiency after pulmonary embolism, lung transplantation, etc. To investigate the role of HSP22 in LIRI mice, ischemia-reperfusion injury was established in the left lung of an HSP22 overexpression transgenic mouse. Twelve HSP22 transgenic (TG) mice and twelve wild-type (WT) mice were randomly divided into 2 groups: the sham-operated group (SO: TG-SO, WT-SO) and the ischemia-reperfusion group (I/R: TG-I/R, WT-I/R), respectively. We tested the PaO2, W/D ratio, and MDA level; observed morphology changes; and calculated the index of alveolar damage. HSP22 expression was examined in lung tissues of TG and WT C57BL mice by immunohistochemistry. TUNEL assay was performed to measure apoptosis. We found that HSP22 was significantly overexpressed in TG mice. There was no difference in PaO2 among the four groups. In the I/R group, the W/D ratio, MDA and index of alveolar damage were higher than those in the SO group. Moreover, compared with WT-I/R group, the W/D ratio, MDA and index of alveolar damage in the TG-I/R group were significantly decreased. Apoptosis in the I/R groups was increased compared to that in the SO groups, while apoptosis in the TG-I/R groups was decreased compared to that in the WT-I/R groups. Our results showed that HSP22 TG mice and the LIRI model were successfully established. In addition, HSP22 overexpression has protective effects on LIRI by inhibiting lipid peroxidation and apoptosis.