Kisspeptin‑13 inhibits bleomycin‑induced pulmonary fibrosis through GPR54 in mice

摘要: Kisspeptin (KP) is an amidated neurohormone that encoded by the KiSS‑1 metastasis suppressor (KISS1) gene and serves as endogenous ligand for G protein‑coupled receptor 54 (GPR54). KP involved in regulation of several biological functions, such reproduction, cancer atherogenesis. Recent data suggested may induce atherosclerotic plaque progression instability, which be reversed GPR54 antagonist KP‑234. Despite KISS1 being previously reported a downstream target classic transforming growth factor (TGF)/Smad2 signaling pathway, its role fibrosis remains elusive. The purpose present study was to evaluate KP‑13 (a product gene) bleomycin (BLM)‑induced idiopathic pulmonary model. Lung tissue samples were evaluated quantitative PCR analysis, western blotting ELISA. Daily intraperitoneal administration significantly ameliorated body weight loss, histopathological lung abnormalities collagen deposition induced BLM. Furthermore, downregulated expression levels tumor necrosis factor‑α, TGF‑β, type I α1, actin α2 matrix metalloproteinase 2 BLM‑treated lungs compared with BLM group. Notably, production α‑smooth muscle tissues, well TGF‑β1 phosphorylated‑Smad2/3, reduced following treatment KP‑13. anti‑fibrotic effects KP‑234 (an GPR54), but not Cetrorelix gonadotropin‑releasing hormone receptor). apoptosis‑related proteins, Bax caspase‑3, decreased, whereas Bcl‑2 markedly increased determined blotting. Collectively, these KP/GPR54 pathway promising fibrosis.