Loureirin A Exerts Antikeloid Activity by Antagonizing the TGF-β1/Smad Signalling Pathway

Abstract

It has been recently shown that loureirin A (LA), a major active component of resina draconis, might be effective in the prevention and treatment of liver fibrosis. We examined whether LA could inhibit the formation of keloids. To investigate the pharmacological effects of loureirin A on keloid formation and the underlying mechanisms. CellTiter-Blue viability assays were used to examine the proliferation of keloid fibroblasts (KFs) that were treated with LA. Fibroblast migration was evaluated using a cell migration assay. Immunofluorescence staining was used to measure the expression of α-SMA in KFs. RT-qPCR was used to evaluate the mRNA expression of Col-I, Col-III, α-SMA, Bax, and Caspase-3, while Western blotting was used to evaluate the protein expression of Col-I, Col-III, α-SMA, Bax, Caspase-3, p-Smad2, and p-Smad3. LA inhibited the proliferation of KFs and suppressed the migration and TGF-β1-induced myofibroblast differentiation of KFs. In addition, LA downregulated the mRNA and protein levels of Col-I, Col-III, and α-SMA while promoting the mRNA and protein levels of Bax and Caspase-3. Moreover, LA downregulated the protein levels of p-Smad2 and p-Smad3 in cultured TGF-β1-treated KFs ex vivo. These results show that LA has an antikeloid effect on KFs by suppressing the TGF-β1/Smad signalling pathway. Our findings suggest that LA may be a potential candidate drug for the prevention and treatment of keloids.

Pharmacotherapy for Keloids and Hypertrophic Scars

“…Loureirin A/B, a major active component of Resina Draconis (Dracaena cochinchinensis), inhibits the proliferation, and suppresses the migration and TGF-β1-induced myofibroblast differentiation, of KD fibroblasts [287][288][289]. Resina Draconis is a type of dragon's blood resin obtained from Dracaena cochinchinensis (Lour.)…”

Retracted: Loureirin A Exerts Antikeloid Activity by Antagonizing the TGF‐β1/Smad Signalling Pathway

“…This article has been retracted by Hindawi, as publisher, following an investigation undertaken by the publisher [ 1 ]. This investigation has uncovered evidence of systematic manipulation of the publication and peer-review process.…”