Emodin, an anthraquinone derivative from Rheum officinale Baill, enhances cutaneous wound healing in rats.

Emodin (1, 3, 8-trihydroxy-6-methyl-anthraquinone) is an anthraquinone derivative from the roots of Rheum officinale Baill, a Chinese herb widely and traditionally used for wound healing. Our objective was to determine whether topically applied emodin enhanced repair of rats' excisional wounds and its possible mechanism. Wounds were treated with either topical emodin (100, 200 and 400 microg/ml), recombinant human epidermal growth factor (rhEGF, 10 microg/ml), or vehicle for 7 or 14 days consecutively. At day 5 postinjury, wounds receiving emodin (400 microg/ml) were significantly smaller than those treated with vehicle. Emodin treatments had markedly more hydroxyproline content in day 7 wounds and tensile strength in day 14 wounds than that of vehicle control. The level of transforming growth factor- beta(1) (TGF-beta(1)) in wound tissues assessed by immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR), showed a dose-dependent increase in emodin-treated wounds compared with vehicle. Western immunoblotting analysis of wound tissues for Smad 2, 3, 4, 7 protein expression showed increase in Smad 2, 3 in the emodin-treated wounds compared with vehicle. In contrast, a reduction of Smad 7 was observed in emodin-treated wounds compared with vehicle and no change of Smad 4. In summary, our results showed that emodin promoted repair of rats' excisional wounds via a complex mechanism involving stimulation of tissue regeneration and regulating Smads-mediated TGF-beta(1) signaling pathway.