Li H-X, Liu H, Wang C-M, Wang H-J, Chen J
General Hospital of Chongqing Iron and Steel Group, Chongqing, China.
Eur Rev Med Pharmacol Sci. 2014;18(21):3199-204.
This study aims to discuss the function and molecular mechanism of artesunate in resisting pulmonary fibrosis.
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.
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).
Artesunate blocks the MAPK cell conduction pathway through Smad7 to restrain idiopathic pulmonary fibrosis.
本研究旨在探讨青蒿琥酯抗肺纤维化的作用及分子机制。
用青蒿琥酯刺激HFL-I细胞系，该细胞系抑制Smad7蛋白表达。在不同条件下，检测所有处理因素，包括Smad7、p-P38、ERK和p-JNK蛋白表达。采用流式细胞术检测细胞周期。对于p-Smad7蛋白的沉默表达，蛋白质免疫印迹分析显示，与未处理组相比，Smad7、p-P38和p-JNK蛋白减少。
青蒿琥酯刺激p-Smad7蛋白表达沉默的细胞后，Smad7、p-P38和p-JNK蛋白无明显变化（p>0.5）。对p-Smad7蛋白表达沉默的细胞使用TGF-β1重组因子后，Smad7、p-P38和p-JNK蛋白表达无明显变化（p>0.5）。
青蒿琥酯通过Smad7阻断MAPK细胞传导通路，抑制特发性肺纤维化。
