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Fig. 1 | Molecular Medicine

Fig. 1

From: The α7 nicotinic acetylcholine receptor agonist, GTS-21, attenuates hyperoxia-induced acute inflammatory lung injury by alleviating the accumulation of HMGB1 in the airways and the circulation

Fig. 1

Systemic administration of GTS-21 decreases lung injury in mice exposed to prolonged hyperoxia. C57BL/6 mice were exposed to either ≥99% O2 for 3 days or 21% O2 (room air). Mice were randomized to receive either GTS-21 (0.04, 0.4 and 4 mg/kg) or saline, administrated by intraperitoneal injection every 8 h starting at 32 h following the onset of hyperoxic exposure. Lungs and BAL were harvested at the end of hyperoxia treatment. a The total protein content in the BAL was measured as a marker of lung injury. b-c Lungs, harvested at the end of hyperoxic exposure, were fixed, embedded and sectioned. Images of the Hematoxylin-eosin-stain of the lung sections from room air samples (RA), and hyperoxic samples from mice treated with either vehicle saline control (0 m/kg) or GTS-21, (4 mg/kg) are shown (b) and their lung histopathological scores assessed (c). Data represent the mean ± SEM from three independent experiments (n = 6–10 mice/group). *p < 0.05, compared with mice receiving normal saline

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Molecular Medicine

ISSN: 1528-3658