Cafestol Inhibits High-Glucose-Induced Cardiac Fibrosis in Cardiac Fibroblasts and Type 1-Like Diabetic Rats

Figure 1

Effects of cafestol on high-glucose-induced cell proliferation, collagen synthesis, TGF-β1 secretion, and Smad2/3 phosphorylation in cardiac fibroblasts. Cardiac fibroblasts were cultured in a serum-free normal glucose medium (5.6 mM glucose) or high-glucose medium (25 mM glucose) in the absence or presence of cafestol (1, 3, 10, 30, or 100 μM) for 24 h. (a) Cell proliferation was assessed using BrdU incorporation. The results are reported as the mean ± SEM (n = 5). (b) Collagen synthesis was assessed using ³H-proline incorporation. The results are reported as the mean ± SEM (n = 5). (c) The secretion level of TGF-β1 in cardiac fibroblasts supernatant was measured using an ELISA assay. The results are reported as the mean ± SEM (n = 6). (d) The protein expression levels of Smad2/3 and P-Smad2/3 were detected using western blotting. Cardiac fibroblasts were treated with a normal glucose medium or high-glucose medium in the absence or presence of cafestol (30 μM) for 2 h. Representative micrograph of the expression of Smad2/3 and P-Smad2/3 in a western blot analysis (upper) and the quantitative results (lower). The results are reported as the mean ± SEM (n = 3). versus normal glucose control group; # versus high-glucose group.

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