Effect of phlorotannins on myofibroblast differentiation and ECM protein expression in transforming growth factor β1‑induced nasal polyp‑derived fibroblasts

Abstract

Phlorotannins (PTNs), a group of phenolic compounds from seaweeds, have diverse bioactivities. However, there has been no report on their antifibrotic effects during nasal polyp (NP) formation. In the present study, the effect of PTNs on transforming growth factor (TGF)‑β1‑induced profibrotic responses in nasal polyp‑derived fibroblasts (NPDFs) were determined and the relevant signaling pathways were investigated. The expression levels of collagen type‑1 (Col‑1) and fibronectin in NP tissues were measured by western blot analysis and immunohistochemistry. The NPDFs were treated with TGF‑β1 (1 ng/ml) in the presence or absence of PTNs (5‑30 µg/ml). The expression levels of α‑smooth muscle actin (α‑SMA), Col‑1, fibronectin, and phosphorylated‑small mothers against decapentaplegic (Smad)2/3 in NPDFs were measured by western blot analysis. The contractile activity of the NPDFs was determined by a collagen gel contraction assay. Col‑1 and fibronectin proteins were found to be expressed in NP tissues. PTNs had no significant cytotoxic effect on TGF‑β1‑induced NPDFs. TGF‑β1 induced the expression α‑SMA, Col‑1 and fibronectin, and stimulated fibroblast‑mediated contraction of collagen gel. However, pre‑treatment with PTNs inhibited the expression of these proteins. The inhibitory effects were mediated through the suppression of Smad2/3 signaling pathways in TGF‑β1‑induced NPDFs. These resulted suggested that PTNs may be important in inhibiting myofibroblast differentiation and extracellular matrix protein accumulation in NP formation through the Smad2/3 signaling pathway.

Benzyl Isothiocyanate Attenuates Inflammasome Activation in Pseudomonas aeruginosa LPS-Stimulated THP-1 Cells and Exerts Regulation through the MAPKs/NF-κB Pathway

“…The final objectives of this research were to verify whether IL-1β produced by endotoxinstimulated activation of inflammasomes induces fibrosis and to reveal the reaction mechanism in the growth of nasal polyps (NPs). NPs are a chronic disease of the nose and sinuses with nasal obstruction, runny nose, smell and taste loss, headache, and a high recurrence rate after medical or surgical treatment, often leading to substantial impairment of the quality of life of the patient [19]. IL-1β is expressed in NPs, and P. aeruginosa is a common culture isolate in chronic rhinosinusitis (CRS) [20].…”

Combined treatment of low‐level laser therapy and phloroglucinol for inhibition of fibrosis

“…PHL has been widely studied and used for pharmaceutical effect to treat gallstones and gastrointestinal disorders . In addition, PHL forms phlorotannin that inhibits fibrosis by modulating the expression of TGF, α‐SMA, and myofibroblast transition . Thus, the application of biocompatible marine‐derived PHL is a feasible material‐based treatment for fibrotic diseases, such as tracheal stenosis.…”

Proteasome inhibitor MG132 inhibits the process of renal interstitial fibrosis

“…Several in vitro studies have determined that CTGF stimulates the proliferation of cardiac fibroblasts and increase the production of the ECM (30,31). Resulting myofibroblasts and tubular epithelial cells have been revealed to produce ECM materials to induce interstitial fibrosis (32). α-SMA is a phenotypic transformation marker that is highly expressed in myofibroblasts, which are widely used as a marker of cell differentiation, while its production simultaneously contributes significantly to fibrosis (33).…”