Objective:
Renal fibrosis is a common pathway leading to the progression of chronic kidney
disease. Activated fibroblasts contribute remarkably to the development of renal fibrosis. Although
apigenin has been demonstrated to play a protective role from fibrotic diseases, its pharmacological effect
on renal fibroblast activation remains largely unknown.
Materials and Methods:
Here, we examined the functional role of apigenin in the activation of renal
fibroblasts response to transforming growth factor (TGF)-β1 and its potential mechanisms. Cultured
renal fibroblasts (NRK-49F) were exposed to apigenin (1, 5, 10 and 20 μM), followed by the stimulation
of TGF-β1 (2 ng/mL) for 24 h. The markers of fibroblast activation were determined. In order to
confirm the anti-fibrosis effect of apigenin, the expression of fibrosis-associated genes in renal fibroblasts
was assessed. As a consequence, apigenin alleviated fibroblast proliferation and fibroblastmyofibroblast
differentiation induced by TGF-β1.
Result:
Notably, apigenin significantly inhibited the fibrosis-associated genes expression in renal fibroblasts.
Moreover, apigenin treatment significantly increased the phosphorylation of AMP-activated
protein kinase (AMPK). Apigenin treatment also obviously reduced TGF-β1 induced phosphorylation
of ERK1/2 but not Smad2/3, p38 and JNK MAPK in renal fibroblasts.
Conclusion:
In a summary, these results indicate that apigenin inhibits renal fibroblast proliferation,
differentiation and function by AMPK activation and reduced ERK1/2 phosphorylation, suggesting it
could be an attractive therapeutic potential for the treatment of renal fibrosis.
Helper cell-independent cytotoxic clones in man.
