Selenomethionine protects against Escherichia coli-induced endometritis by inhibiting inflammation and necroptosis via regulating the PPAR-γ/NF-κB pathway

• Published in: Chemico-biological interactions Vol. 379; p. 110532
• Main Authors: Cao, Lu, Gao, Shouyang, Liu, Junbao, Wang, Junrong, Qin, Rui
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier B.V 01.07.2023
• Subjects: Endometritis; Endometritis - chemically induced; Endometritis - metabolism; Endometritis - prevention & control; Escherichia coli - metabolism; Female; Humans; Inflammation; Inflammation - prevention & control; Lipopolysaccharides; Necroptosis; NF-kappa B - metabolism; PI3K; PPAR gamma; Selenomethionine; Selenomethionine - adverse effects; Inflammation; PI3K; Necroptosis; Endometritis; Selenomethionine
• ISSN: 0009-2797; 1872-7786
• DOI: 10.1016/j.cbi.2023.110532

Endometritis, inflammation of the endometrium, is a major cause of subfertility in women. Selenomethionine (SeMet)is known to exert anti-inflammatory activity. We aimed to verify the protective roles of SeMet on Escherichia coli (E.coli)-induced endometritis. The extent of uterus damage was assessed by detecting histopathology and inflammatory mediators. The results revealed that SeMet significantly prevented E.coli-induced endometritis by attenuating uterine histopathology and inflammatory cytokine production. E.coli-induced MPO activity and MDA content were inhibited by SeMey. E.coli-induced ZO-1 and occludin were upregulated by SeMet. E.coli-induced necroptosis was also inhibited by SeMet. Additionally, E.coli-induced NF-κB activation was alleviated by SeMet. PPAR-γ expression was upregulated by SeMet. Notably, the protective effects of SeMet on endometritis were abolished by a PPAR-γ inhibitor. In conclusion, SeMet inhibits E.coli-induced endometritis by attenuating inflammation and necroptosis, which is mediated by the PPAR-γ/NF-κB signaling pathway. •SeMet significantly prevented E.coli-induced endometritis through attenuating uterus histopathology.•E.coli-induced ZO-1 and occludin was downregulated by SeMet.•E.coli-induced necroptosis was also inhibited by SeMet.•E.coli-induced NF-κB activation was suppressed by SeMet and the expression of PPAR-γ was up-regulated by SeMet.