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Effect of asiaticoside on hypertrophic scar in the rabbit ear model

Background:  Previous observations suggested that asiaticoside had a possible antiscaring effect. However, the precise pathological mechanism still remain unknown. We questioned whether asiaticoside might alleviate the formation of hypertrophic scar by affecting the expression of Transform growth fa...

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Published in:Journal of cutaneous pathology 2009-02, Vol.36 (2), p.234-239
Main Authors: Ju-lin, Xie, Shao-hai, Qi, Tian-zeng, Li, Bin, Huang, Jing-ming, Tang, Ying-bin, Xu, Xu-sheng, Liu, Bin, Shu, Hui-zhen, Liang, Yong, Huang
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Language:English
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Summary:Background:  Previous observations suggested that asiaticoside had a possible antiscaring effect. However, the precise pathological mechanism still remain unknown. We questioned whether asiaticoside might alleviate the formation of hypertrophic scar by affecting the expression of Transform growth factor β (TGF‐β)/Smad signaling. Aims:  To investigate the effect of asiaticoside on the expression of TGF‐β/Smad signaling in the rabbit ear model of hypertrophic scar and to clarify the mechanism of asiaticoside on the scar treatment. Methods:  The rabbit model with hypertrophic scar was created and applied topically with a low‐dose (0.5%) or high‐dose (1%) asiaticoside three times daily for 1, 2 or 3 months and then we examined the changes of macroscopic and histopathologic characteristics of scars, and the expression of TGF‐β1 and Smad protein was studied by applying reverse transcription‐polymerase chain reaction and western blotting. Result:  Asiaticoside could remarkably alleviate the scar in the rabbit ear model. Western blotting showed that the asiaticoside could decrease TGF‐β1 expression, and further study revealed that asiaticoside could remarkably enhance the expression of inhibitory Smad7, but it had no effect on the expression of Smad2. Conclusion:  Asiaticoside suggested a possible antiscaring effect probably by enhancing the expression of inhibitive Smad7.
ISSN:0303-6987
1600-0560
DOI:10.1111/j.1600-0560.2008.01015.x