ArticleImmunity, inflammation and disease2023
TNFAIP3 interacting protein 2 relieves lipopolysaccharide (LPS)-induced inflammatory injury in endometritis by inhibiting NF-kappaB activation.
Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Atractylenolide II alleviates LPS-induced acute lung injury in A549 cells via the TNIP2/NF-κB pathway.Journal of cardiothoracic surgery · 2026Article
- Uterine inflammation and lessons from large animal models of endometritis.Nature reviews. Immunology · 2025Review
- Ionizing radiation-induced disruption of Rela-Bclaf1-spliceosome regulatory axis in primary spermatocytes causing spermatogenesis dysfunction.Cell communication and signaling : CCS · 2025Article
- An Overview of Bioactive Compounds' Role in Modulating the Nrf2/Keap1/NF-κB Pathway to Alleviate Lipopolysaccharide-Induced Endometritis.International journal of molecular sciences · 2024Review
- TNFAIP3 interacting protein 2 relieves lipopolysaccharide (LPS)-induced inflammatory injury in endometritis by inhibiting NF-kappaB activation.Immunity, inflammation and disease · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
backgroundEndometritis 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.
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