[The anti-inflammatory effects of heme oxygenase-1 on emphysema model]

The effects of HO-1 on smoke-induced emphysema were tested and the mechanisms were explored in a smoking rat model.

In this study, rats were either exposed or sham-exposed to cigarette smoke for emphysema modeling. Hemin were injected during this period to induce HO-1. Subsequently, emphysema development, inflammatory cells and cytokine levels were analyzed.

Smoke exposure induced emphysema [MLI: (34.0 ± 2.2) µm, MAN: 2.3 ± 0.5, MAA: (0.5 ± 0.1) µm²], increased the inflammatory cells count [total number: (41.0 ± 13.9) × 10⁴/ml, Neutrophil: (25.0 ± 9.8) × 10⁴/ml, Macrophage: (7.2 ± 2.8) × 10⁴/ml] and inflammatory cytokine levels especially IL-17 [serum: (33 ± 8.4) pg/ml, lung tissue homogenate: (79 ± 7) pg/ml, BALF: (39 ± 8) pg/ml], IL-8 [serum: (181 ± 51) pg/ml, BALF: (162 ± 79) pg/ml] and TNF-α [serum: (607 ± 85) pg/ml, BALF: (504 ± 223) pg/ml]. HO-1 reduced the severity of emphysema [MLI: (28.6 ± 1.1) µm, MAN: (2.7 ± 0.7), MAA: (0.4 ± 0.1) µm²]; total number: (17.6 ± 5.6) × 10²/ml, Neutrophil: (10.2 ± 3.6) × 10²/ml, Macrophage: (2.6 ± 1.1) × 10²/ml, suppressed the secretion of IL-17 [serum: (23.9 ± 2.4) pg/ml, lung tissue homogenate: (69.2 ± 3.0) pg/ml, BALF: (17.8 ± 5.3) pg/ml], IL-8 [serum:(103 ± 50) pg/ml, BALF: (114 ± 35) pg/ml] and TNF-α [serum: (423 ± 48) pg/ml, BALF: (216 ± 134) pg/ml] and prevented emphysema development.

HO-1 has anti-inflammatory effects and can prevent smoke-induced emphysema development.