Mitigative effect of Naringenin in bleomycin induced systemic sclerosis model; role of Notch signaling pathway

Abstract

Background An immunological, proinflammatory, and vascular disorder called systemic sclerosis (SSc) frequently leading to progressive tissue fibrosis. Reactive oxidizing species are thought to have a substantial influence on disease initiation and progression, based on a variety of studies. Also, Notch signaling is known to modulate fibroblast homeostasis, angiogenesis, and lymphocyte development. Aim This experimental study was designed to shed light on the possible ameliorating mechanism of naringenin as antioxidant in bleomycin-induced SSc model via focusing on Notch signaling cascade. Materials and methods 50 male albino mice were employed for the test, while being allocated randomly to one of five equal groups as follows: Control group (group I), Naringenin-treated group (group II), Bleomycin-treated group (group III), and group IV (Naringenin/Bleomycin co-treated group) and group V (Bleomycin followed by Naringenin treated group). Plasma hydrogen peroxide level, skin tissue hydrogen peroxide and hydroxyproline levels were measured using colorimetric assay. A Disintegrin and metalloproteinase domain containing protein 17 and neuregulin 1 levels in skin tissue were measured by Enzyme-linked immunosorbent assay. Histological evaluation was also performed. Results Plasma hydrogen peroxide, skin tissue hydrogen peroxide, hydroxyproline, a Disintegrin and metalloproteinase domain containing protein 17 and neuregulin 1 levels in the bleomycin-treated group were significantly increased than other studied groups. Naringenin administration in parallel with the induction mitigated the obtained biochemical changes and protected against the chemical induction of SSc. Conclusion Naringenin could protect against bleomycin-induced SSc through its antioxidant role.