Protective Effect of Low-Molecular-Weight Fucoidan on Radiation-Induced Fibrosis Through TGF-β1/Smad Pathway-Mediated Inhibition of Collagen I Accumulation.
Radiation-induced fibrosis (RIF) occurs after radiation therapy in normal tissues due to excessive production and deposition of extracellular matrix proteins and collagen, possibly resulting in organ function impairment. This study investigates the effects of low-molecular-weight fucoidan (LMF) on irradiated NIH3T3 cells. Specifically, we quantified cellular metabolic activity, fibrosis-related mRNA expression, transforming growth factor beta-1 (TGF-β1), and collagen-1 protein expression, and fibroblast contractility in response to LMF. LMF pre + post-treatment could more effectively increase cellular metabolic activity compared with LMF post-treatment. LMF pre + post-treatment inhibited TGF-β1 expression, which mediates negative activation of phosphorylated Smad3 (pSmad3) and Smad4 complex formation and suppresses downstream collagen I accumulation. In addition, LMF pre + post-treatment significantly reduced actin-stress fibers in irradiated NIH3T3 cells. LMF, a natural substance obtained from brown seaweed, may be a candidate agent for preventing or inhibiting RIF.
['Wu|Szu-Yuan|SY|0000-0001-5637-558X', 'Chen|Yu-Ting|YT|', 'Tsai|Guo-Yu|GY|', 'Hsu|Fu-Yin|FY|', 'Hwang|Pai-An|PA|']
D000818:Animals D003094:Collagen D051379:Mice D041681:NIH 3T3 Cells D011134:Polysaccharides D020011:Protective Agents D017564:Radiation Pneumonitis D015398:Signal Transduction D051900:Smad3 Protein D016212:Transforming Growth Factor beta
low-molecular-weight fucoidan radiation-induced fibrosis TGF-β1 collagen I Smad pathway