Figure 3
From: Deficiency of α7 Nicotinic Acetylcholine Receptor Attenuates Bleomycin-Induced Lung Fibrosis in Mice
Effect of α7 nAChR on body-weight loss, lung fibrogenic and proinflammatory genes during the development of BLM-induced lung fibrosis. (A) Effect α7 nAChR on body-weight loss during the development of BLM-induced lung fibrosis. Chrna7+/+ and Chrna7−/− mice were intratracheally challenged with BLM (1.5 mg/kg) and followed for 14 d. N = 18–20 in each group. *p < 0.05 for Chrna7+/+ versus Chrna7−/− mice receiving intratracheal BLM. Data are mean ± SD. (B-D) Effect of α7 nAChR on lung fibrogenic genes during the development of BLM-induced lung fibrosis. Experimental protocol was the same as Figure 3A. The mice were euthanized at 7 d and the lungs were homogenized for extracting RNA to measure (B) Col1a1, (C) Fsp1 and (D) Fstl1 by qPCR analysis. N = 3–6 in each group. *p < 0.05, **p < 0.01, ***p < 0.001 in each gene comparison for Chrna7+/+versus Chrna7−/− mice receiving intratracheal BLM. (E-G) Effect of α7 nAChR on lung proinflammatory genes during the development of BLM-induced lung fibrosis. Experimental protocol was the same as Figures 2B-D. The lungs were homogenized for extracting RNA to measure (E) Cxcl2, (F) Mcp1 and (G) Arg1 by qPCR analysis. N = 3–5 in each group. ***p < 0.001 in each gene comparison for Chrna7+/+ versus Chrna7−/− mice receiving intratracheal BLM. Data are mean ± SD.