Sulforaphane modulates TGFβ2-induced conjunctival fibroblasts activation and fibrosis by inhibiting PI3K/Akt signaling

• 作者: Han-Ruo Liu Ning-Li Wang Zi-Yao Xia
• 来源期刊: 国际眼科杂志:英文版
• 学科: 医学
• 关键词: human conjunctival fibroblasts SULFORAPHANE transforming growth factorβ2 PI3K/Akt signaling
• 年，卷（期）: 2020,（10）
• 页码范围: 1505-1511
• 页数: 7页
• 分类号: R965

摘要

AIM:To examine the effects of sulforaphane on fibrotic changes of transforming growth factor(TGFβ2)induced human conjunctival fibroblast(HCon Fs).METHODS:HCon Fs were cultured and divided into control,TGFβ2(1 ng/m L),sulforaphane and TGFβ2+sulforaphane groups.Cell viability and apoptosis were detected using the MTT and Apo Tox-Glo Triplex assay.Cell migration was detected using scratch and Transwell assay.Real-time quantitative PCR method was used to evaluate m RNA expression of TGFβ2,matrix metalloproteinase-2(MMP2),myosin light chain kinase(MYLK),integrinαV,integrinα5,fibronectin 1 andα-smooth muscle actin(α-SMA).The protein expression ofα-SMA,p-PI3 K,PI3 K,p-Akt,and Akt were detected by Western blot.RESULTS:The proliferation of HCon Fs was significantly(P<0.05)suppressed by sulforaphane compared to control cells with the increase of the concentration and treatment time.Cell proliferation after 48 h incubation was significantly reduced with 100μmol/L sulforaphane treatment by 17.53%(P<0.05).The Transwell assay showed sulforaphane decreased cell migration by 18.73%compared with TGFβ2-induced HCon F(P<0.05).TGFβ2-induced the increasing expression of fibronectin,type I collagen andα-SMA,and the phosphorylation of PI3 K and Akt were all significantly suppressed by sulforaphane pretreatment.CONCLUSION:Sulforaphane inhibits proliferation,migration,and synthesis of the extracellular matrix in HCon Fs,and inhibiting the PI3 K/Akt signaling pathway.Sulforaphane could be a potential therapeutic drug for prevention of scar formation in filtering bleb after trabeculectomy.