1. Academic Validation
  2. Swainsonine inhibits proliferation and collagen synthesis of NIH-3T3 cells by declining miR-21

Swainsonine inhibits proliferation and collagen synthesis of NIH-3T3 cells by declining miR-21

  • Artif Cells Nanomed Biotechnol. 2019 Dec;47(1):2256-2264. doi: 10.1080/21691401.2019.1620255.
Chao Li 1 Peipei Wang 1 Ziyang Fu 1 Yongtao Li 1 Shouju Li 1
Affiliations

Affiliation

  • 1 a Department of Burn and Plastic Surgery, Heze Municipal Hospital , Heze , China.
Abstract

Swainsonine (SW) is an indolizidine alkaloid first discovered in Swainsona canescens. This study explored the effects of SW on mouse embryo fibroblast NIH-3T3 cell proliferation and collagen synthesis, as well as potential molecule mechanisms. We discovered that SW exposure lowered the viability and proliferation of NIH-3T3 cells. The collagen synthesis was reduced after SW exposure, as evidenced by declines of the mRNA and protein levels of collagen I (CoI I), collagen III (CoI III) and α-smooth muscle actin (α-SMA) in NIH-3T3 cells, as well as reduction of collagen concentration in the culture supernatant of NIH-3T3 cells. Mechanically, transforming growth factor β1 (TGF-β1) stimulation elevated the microRNA-21 (miR-21) expression in NIH-3T3 cells. SW reversed the TGF-β1-caused elevation of miR-21. Up-regulation of miR-21 attenuated the inhibitory influences of SW on NIH-3T3 cell viability, proliferation and collagen synthesis. Silence of miR-21 had converse influence. Besides, SW inactivated PI3K/Akt and NF-κB pathways via declining miR-21. Altogether, SW inhibited the proliferation and collagen synthesis of fibroblast NIH-3T3 might be through declining miR-21 and then suppressing PI3K/Akt and NF-κB pathways. SW may be an effective therapeutic medicine for scar hyperplasia.

Keywords

NF-κB pathway; PI3K/AKT pathway; Scar hyperplasia; Swainsonine; fibroblasts; microRNA-21.

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