Emphysema is a serious disease of the respiratory system and is associated with
inflammation and oxidative stress.
Heme oxygenase-1 (HO-1), a rate-limiting
enzyme involved in
heme biosynthesis, exerts potent anti-inflammatory,
antioxidant, anti-apoptotic and anti‑proliferative effects in various diseases. In the present study, we examined the effects of HO-1 on smoke‑induced
emphysema, as well as the underlying mechanisms in a rat model of
smoke-induced
emphysema. Rats were either exposed to cigarette
smoke or sham‑exposed for 20 weeks to establish the model of
smoke-induced
emphysema. The rats were subcutaneously injected with
protoporphyrin IX [
tin-protoporphyrin IX (SnPP) or
ferriprotoporphyrin IX chloride (
hemin)] during this period to examine the protective effects of HO-1. Subsequently, the development of
emphysema, inflammatory cells, the levels of inflammatory mediators, particularly
interleukin (IL)-17,
tumor necrosis factor (TNF)‑α, monocyte chemotactic protein‑1 [MCP‑1, also known as
chemokine (C-C motif) ligand 2 (CCL2)],
IL-8 [also known as
chemokine (C-X-C motif)
ligand 8 (CXCL8)], macrophage inflammatory protein‑2α [MIP-2α, also known as
chemokine (C-X-C motif) ligand 2 (CXCL2)] and
IL-10, as well as the
malondialdehyde (MDA),
superoxide dismutase (SOD) and
glutathione (GSH) content were determined. Exposure to
smoke increased the total cell, neutrophil and macrophage counts in the bronchoalveolar lavage fluid (BALF). It also increased the levels of the inflammatory mediators,
IL-17, TNF-α, MCP-1,
IL-8 and MIP-2α, as well as the MDA content and induced
emphysema. Treatment with
hemin upregulated HO-1 expression and attenuated the development of
smoke-induced
emphysema by reducing inflammatory cell infiltration, decreasing the levels of inflammatory mediators and attenuating oxidative damage, to a certain extent. In conclusion, our findings demonstrate that HO-1 exerts anti-inflammatory and
antioxidant effects, thus attenuating the development of
smoke-induced
emphysema.