The Inhibition Effect and Mechanism of Staurosporine Isolated from Streptomyces sp. SNC087 Strain on Nasal Polyp.
Grace ChoiEun-Young LeeDawoon ChungKichul ChoWoon-Jong YuSang-Jip NamSeong-Kook ParkIl-Whan ChoiPublished in: Marine drugs (2024)
This study aims to explore the potential inhibition effects of staurosporine isolated from a Streptomyces sp. SNC087 strain obtained from seawater on nasal polyps. Staurosporine possesses antimicrobial and antihypertensive activities. This research focuses on investigating the effects of staurosporine on suppressing the growth and development of nasal polyps and elucidating the underlying mechanisms involved. The experimental design includes in vitro and ex vivo evaluations to assess the inhibition activity and therapeutic potential of staurosporine against nasal polyps. Nasal polyp-derived fibroblasts (NPDFs) were stimulated with TGF-β1 in the presence of staurosporine. The levels of α-smooth muscle actin (α-SMA), collagen type-I (Col-1), fibronectin, and phosphorylated (p)-Smad 2 were investigated using Western blotting. VEGF expression levels were analyzed in nasal polyp organ cultures treated with staurosporine. TGF-β1 stimulated the production of Col-1, fibronectin, and α-SMA and was attenuated by staurosporine pretreatment. Furthermore, these inhibitory effects were mediated by modulation of the signaling pathway of Smad 2 in TGF-β1-induced NPDFs. Staurosporine also inhibits the production of VEGF in ex vivo NP tissues. The findings from this study will contribute to a better understanding of staurosporine's role in nasal polyp management and provide insights into its mechanisms of action.
Keyphrases
- chronic rhinosinusitis
- transforming growth factor
- signaling pathway
- smooth muscle
- epithelial mesenchymal transition
- gene expression
- endothelial cells
- poor prognosis
- blood pressure
- staphylococcus aureus
- vascular endothelial growth factor
- high resolution
- oxidative stress
- pi k akt
- cell proliferation
- climate change
- induced apoptosis
- diabetic rats
- binding protein
- high glucose
- endoplasmic reticulum stress
- cell migration
- molecularly imprinted