Artesunate restraining MAPK passage by smad7 to resist pulmonary fibrosis

H.-X. Li, H. Liu C.-M. Wang, H.-J. Wang, J. Chen

General Hospital of Chongqing Iron and Steel Group, Chongqing, China. changmingwangcn@163.com

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• Respiratory Medicine

OBJECTIVES: This study aims to discuss the function and molecular mechanism of artesunate in resisting pulmonary fibrosis.

METHODS: Artesunate was used to stimulate the HFL-I cell line, which restrains the expression of Smad7 protein. Under different conditions, all treatment factors were checked, including Smad7, p-P38, ERK, and p-JNK protein expressions. Flow cytometry was used to detect the cell cycle. For the silent expression of the p-Smad7 protein, Western blot analysis revealed that Smad7, p-P38, and p-JNK proteins decreased compared with those of the non-treatment group.

RESULTS: No significant changes were observed in Smad7, p-P38, and p-JNK proteins after the cells with silent p-Smad7 protein expression were stimulated by artesunate (p > 0.5). No significant changes were observed in the expression of Smad7, p-P38, and p-JNK proteins after using TGF-β1 recombination factor to cells whose p-Smad7 protein expression is silent (p > 0.5).

CONCLUSIONS: Artesunate blocks the MAPK cell conduction pathway through Smad7 to restrain idiopathic pulmonary fibrosis.

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