LAUSR

BACKGROUND Scars affects the appearance and results in tissue damage. In this research, we preliminarily studied the function and mechanism of curcumin (CUR) on cell proliferation and soluble collagen synthesis in NIH-3T3 cells. METHODS CCK-8 was used to detect the IC50 of CUR. Moreover, Western blot was used to measure the expression of cell proliferation-related, soluble collagen synthesis and pathway-related proteins. Sircol assay was determined the expression of soluble collagen. Furthermore, reverse transcription quantitative PCR (RT-qPCR) was used to determined miR-29a, α-smooth muscle aorta (α-SMA), soluble collagen 1 (Col 1) and Col 3 expression. RESULTS CUR inhibited cell viability and proliferation-related proteins expression. Transforming growth factor-β (TGFβ1)-induced heightened the expression of proliferation-related proteins and soluble collagen synthesis-related proteins. CUR inhibited TGFβ1-induced proliferation and soluble collagen synthesis. Furthermore, CUR positively related miR-29a and miR-29a mimic inhibited TGFβ1-induced proliferation and soluble collagen synthesis. Besides, transfection with miR-29a inhibitor could partly reverse the effects of CUR. CUR inhibited the ERK1/2 and β-catenin pathways and the miR-29a inhibitor reversed the above results. Otherwise, soluble collagen 1 (Col 1) partly reversed the effects of CUR on proliferation and soluble collagen synthesis and silenced Col 1/3 could inhibit ERK1/2 and β-catenin signaling pathways. CONCLUSION CUR restrained TGFβ1-induced proliferation and soluble collagen synthesis in NIH-3T3 cells by up-regulation of miR-29a via ERK1/2 and β-catenin signaling pathways.