Blocking TGF-β type 1 receptor partially reversed skin tissue damage in experimentally induced atopic dermatitis in mice.

摘要: Abstract Animals with impaired transforming growth factor (TGF)-β1 signaling developed spontaneous lethal autoimmune inflammation and diseases. Moreover, evidence for modified TGF-β in atopic dermatitis (AD) exists. Therefore, the goal of this study was to determine whether SB-431542, a potent and selective inhibitor type 1 receptor (TGF-βR1), could attenuate such severe reaction mice. In addition, molecular underpinnings possible protective effects were also investigated. Repeated epicutaneous application DNCB performed on ear shaved dorsal skin mice to induce AD-like symptoms lesions. SB-431542 (1 mg/kg) given by intra-peritoneal injection three times weekly 3 weeks assess anti-pruritic effects. Serum levels TGF-β1, TGF-βR1, latency-associated peptide (LAP), tumor necrosis (TNF)-α, interleukin (IL)-1β IL-6 assessed ELISA. gene expression TNF-α, IL-1β determined. Apoptotic pathway evaluated measuring activity caspase-3 staining sections anti-caspase-3 antibodies. We found that alleviated DNCB-induced as quantified lesion, dermatitis score, thickness scratching behavior. parallel, blocked elevation serum LAP, IL-1β, IgE. The collective results indicate partially suppresses AD mice via reduction TGF-β1 associated inhibition inflammation apoptosis.