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Fig. 4 | Molecular Medicine

Fig. 4

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. 4

The sytemic administration of GTS-21 inhibits the infiltration of CD11b+ monocytes/macrophages in the lungs of mice exposed to hyperoxia. C57BL/6 mice were exposed to ≥99% O2 and treated with vehicle (0 mg/kg) or GTS-21 (4 mg/kg) as described in Fig. 1. The lungs were perfused with sucrose, frozen in OCT and cryosectioned. Immunohistochemistry was performed to detect CD11b. a Representative images of lung sections showing DAB positive cells from either control or GTS-21-treated mice. b The total number of CD11b positive DAB stain per field. BAL was harvested at the end of hyperoxia exposure. c-d Cells from the BAL and blood samples were labeled with CD11b and Ly6c antibodies and analyzed by flow cytometry. c Gating for CD11b+ and Ly6c cells in the BAL is shown. d The quantification of the total number of CD11b+ and Ly6c+ in BAL and blood samples analyzed by flow cytometry. Data represent the mean ± SEM from two independent experiments (n = 4 mice/group)

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