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.

中文翻译：

---

姜黄素通过调节 miR-29a 和通过 ERK1/2 和 β-连环蛋白途径抑制 NIH/3T3 细胞系的增殖和可溶性胶原合成。

背景技术疤痕影响外观并导致组织损伤。本研究初步研究了姜黄素（CUR）对NIH-3T3细胞增殖和可溶性胶原合成的作用及机制。方法CCK-8用于检测CUR的IC50。此外，Western印迹用于测量细胞增殖相关、可溶性胶原合成和通路相关蛋白的表达。Sircol法测定可溶性胶原蛋白的表达。此外，逆转录定量 PCR (RT-qPCR) 用于确定 miR-29a、α-平滑肌主动脉 (α-SMA)、可溶性胶原蛋白 1 (Col 1) 和 Col 3 的表达。结果 CUR 抑制细胞活力和增殖相关蛋白的表达。转化生长因子-β (TGFβ1) 诱导的增殖相关蛋白和可溶性胶原合成相关蛋白的表达增加。CUR 抑制 TGFβ1 诱导的增殖和可溶性胶原合成。此外，CUR 正相关的 miR-29a 和 miR-29a 模拟物抑制 TGFβ1 诱导的增殖和可溶性胶原合成。此外，转染 miR-29a 抑制剂可以部分逆转 CUR 的作用。CUR 抑制了 ERK1/2 和 β-catenin 通路，而 miR-29a 抑制剂逆转了上述结果。否则，可溶性胶原蛋白 1 (Col 1) 部分逆转了 CUR 对增殖和可溶性胶原蛋白合成的影响，并且沉默的 Col 1/3 可以抑制 ERK1/2 和 β-连环蛋白信号通路。