TNFAIP3 interacting protein 2 relieves lipopolysaccharide (LPS)‐induced inflammatory injury in endometritis by inhibiting NF‐kappaB activation

Abstract

AbstractBackgroundEndometritis seriously affects the health of women, and it is important to identify new targets for its treatment.ObjectiveThis study aimed to explore the role of TNFAIP3 interacting protein 2 (TNIP2) in endometritis through human endometrial epithelial cells (hEECs) stimulated by lipopolysaccharide (LPS).MethodshEECs were induced with LPS to build a cellular model of endometritis. Cell growth and apoptosis were detected by cell counting kit‐8 and flow cytometry. The TNIP2 mRNA and protein levels were measured using reverse transcription quantitative polymerase chain reaction (RT‐qPCR) and western blot analysis, respectively. The caspase3 activity was calculated using a Caspase3 activity kit. Interleukin (IL)−1β, IL‐6, and tumor necrosis factor‐alpha (TNF‐α) levels were determined by enzyme‐linked‐immunosorbent‐assay. The reactive oxygen species (ROS), lactate dehydrogenase (LDH), catalase (CAT), and superoxide dismutase (SOD) levels were determined using the corresponding kits. Nuclear factor‐kappaB (NF‐κB) pathway was determined by western blot assay.ResultsTNIP2 was downregulated in the LPS‐induced endometritis cell model. Cell viability was reduced, apoptosis was enhanced, and IL‐6, IL‐1β, and TNF‐α levels increased in LPS‐induced hEECs. Additionally, LDH activity and ROS concentration were upregulated, whereas CAT and SOD activities were downregulated in LPS‐induced hEECs. These results were reversed by TNIP2 overexpression. Moreover, the results hinted that NF‐κB was involved in the effects of TNIP2 on the LPS‐induced endometritis cell model.ConclusionTNIP2 alleviated endometritis by inhibiting the NF‐κB pathway, suggesting a potential therapeutic target for endometritis.