S۱۰۰A۹ aggravates bleomycin-induced dermal fibrosis in mice via activation of ERK۱/۲ MAPK and NF-κB pathways

Objective(s): This study aims to investigate the pathogenicity and possible mechanisms of S۱۰۰A۹ function in mice models of scleroderma. Materials and Methods: The content of S۱۰۰A۹ in the skin tissues of mice with scleroderma was determined. Different concentrations of bleomycin (BLM) and S۱۰۰A۹ were subcutaneously injected into the backs of mice simultaneously, and then pathological changes in the skin of these mice were monitored. Specifically, the levels of inflammatory cytokines and alpha smooth muscle actin (α-SMA), the activation of extracellular regulated kinase ۱/۲ (ERK۱/۲), mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) pathways, and the expression of the receptor for advanced glycation end-product (RAGE) in the skin were determined. Results: The content of S۱۰۰A۹ in the skin tissues of mice with scleroderma was determined. Different concentrations of BLM and S۱۰۰A۹ were subcutaneously injected into the backs of mice simultaneously, and then pathological changes in the skin of these mice were monitored. Specifically, the levels of inflammatory cytokines and alpha smooth muscle actin (α-SMA), the activation of extracellular regulated kinase ۱/۲ (ERK۱/۲) mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) pathways, and the expression of the receptor for advanced glycation end-product (RAGE) in the skin were determined. Conclusion: S۱۰۰A۹ aggravates dermal fibrosis in BLM-induced scleroderma (BIS ) mice, and its mechanisms might be mediated by RAGE, ERK۱/۲, and NF-κB pathway.

کلیدواژه ها:

S۱۰۰A۹ ، Scleroderma ، Bleomycin ، RAGE ، ERK۱/۲ MAPK ، NF-κB