Fig. 1.

Chronic nicotine (NIC) exposure augments mediators and markers of inflammation and fibrosis in the postischemic kidney. A group of mice received nicotine in their drinking water for 4 wk while another group received the vehicle (2% saccharine) for the same time as described in materials and methods. Some mice underwent 18-min warm renal ischemia while others were sham operated. Kidneys were collected 24 h postischemia and lysed in RIPA buffer. Transforming growth factor (TGF)-β1 and monocyte-chemotactic protein (MCP)-1 content was determined by ELISA (A) and α-smooth muscle actin (SMA), fibronectin (fibro), and E-cadherin (Ecad) expression along with actin by Western blotting (B). C: densitometry results of Western blots in B. Protein expression was normalized to actin; n = 4 (sham) and n = 8 [ischemia-reperfusion (IR)]. *P < 0.05 compared with sham. #P < 0.05 compared with the corresponding value in the saccharine group.