Fig. 3.

Effects of CS extract (CSE) on fibroblast proliferation and role of nicotinic acetylcholine receptors (nAChRs). Cardiac fibroblasts isolated from rats were quiesced for 24 h, exposed to CSE for 24 h. CSE dose dependently increases cell count (n = 5) (A) and cell viability (B), as assessed by 3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide (MTT) assay (n = 5). C: CSE increases expression of proliferation marker proliferating cell nuclear antigen (PCNA) (n = 9). Data were normalized to vinculin for loading control. D: CSE-induced cell proliferation in cardiac fibroblasts was not attenuated by activation of aldehyde dehydrogenase (Alda-1, 25 μM) or reactive oxygen species (ROS) scavenging (N-acetyl cysteine, NAC, 25 mM) (n = 5). E: mecamylamine (Mec, 20 μM) inhibited CSE-induced fibroblast proliferation (n = 5). Data are normalized to vehicle (Veh) and presented as means ± SE. *P < 0.05 compared with Veh; #P < 0.05 compared with CSE alone.