ArticleJournal of cellular physiology2019
Inhibition of HMGB1 improves necrotizing enterocolitis by inhibiting NLRP3 via TLR4 and NF-κB signaling pathways.
Article in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
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Who cites it
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 119 citations in OpenAlex.
- Targeting TREM2 for Parkinson's Disease: Where to Go?Frontiers in immunology · 2021Pooled it
- Urolithin A attenuates inflammation and enhances barrier integrity in an experimental NEC-in-a-Dish model.Pediatric research · 2026Article
- The role of NLRP3 inflammasome in necrotizing enterocolitis.Pediatric research · 2026Review
- Dualistic Roles of High Mobility Group Box 1 in Cancer and Inflammation.Cancer medicine · 2025Review
- Targeting α‑Klotho Protein by Agmatine and Pioglitazone Is a New Avenue against Diabetic Nephropathy.ACS pharmacology & translational science · 2025Article
- Berberine alleviates respiratory syncytial virus (RSV)-induced pediatric bronchiolitis and fibrosis via suppressing the HMGB1/TLR4/NF-κB pathway.Microbiology spectrum · 2025Article
- Inhibition of NLRP3 Inflammasome Alleviates Postoperative Cognitive Impairment by Suppressing the HMGB-1/TLR4/NF-κB Pathway.Neurochemical research · 2025Article
- Spatial transcriptomics delineates potential differences in intestinal phenotypes of cardiac and classical necrotizing enterocolitis.iScience · 2025Article
- Epigenetic Insights Into Necrotizing Enterocolitis: Unraveling Methylation-Regulated Biomarkers.Inflammation · 2025Article
- Matrine: A Promising Treatment for Ulcerative Colitis by Targeting the HMGB1/NLRP3/Caspase-1 Pathway.Combinatorial chemistry & high throughput screening · 2025Article
- 1-methylnicotinamide attenuated inflammation and regulated flora in Necrotizing enterocolitis.PloS one · 2025Article
- Bone marrow-derived mesenchymal stromal cells in necrotizing enterocolitis treatment: a narrative review.Frontiers in pediatrics · 2025Review
- PhoP/PhoQ Two-Component System Contributes to Intestinal Inflammation Induced byFoods (Basel, Switzerland) · 2024Article
- Modulation of intestinal TLR4 expression in infants with neonatal opioid withdrawal syndrome.Journal of perinatology : official journal of the California Perinatal Association · 2024Article
- Diagnostic significance of serum levels of serum amyloid A, procalcitonin, and high-mobility group box 1 in identifying necrotising enterocolitis in newborns.World journal of gastrointestinal surgery · 2024Article
- NLRP3 activation in macrophages promotes acute intestinal injury in neonatal necrotizing enterocolitis.World journal of pediatrics : WJP · 2024Article
- Increased expression of NLRP3 associated with elevated levels of HMGB1 in children with febrile seizures: a case-control study.BMC pediatrics · 2024Article
- Cynaroside ameliorates methotrexate-induced enteritis in rats through inhibiting NLRP3 inflammasome activation.Frontiers in immunology · 2024Article
- Chromatin as alarmins in necrotizing enterocolitis.Frontiers in immunology · 2024Review
- Glycyrrhizin as a potential disease-modifying therapy for epilepsy: insights into targeting pyroptosis to exert neuroprotective and anticonvulsant effects.Frontiers in pharmacology · 2024Article
3 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo explore the relationship between high-mobility group box 1 (HMGB1) and NLR pyrin domain containing 3 (NLRP3) in the development of necrotizing enterocolitis (NEC).
methodsNEC rat models were constructed and treated with HMGB1 inhibitor glycyrrhizin (GL) with different concentration. An inflammatory condition of intestinal tissue in newborn NEC rats was observed by hematoxylin and eosin staining. The messenger RNA (mRNA) and protein expression of HMGB1, NLRP3, toll-like receptor 4 (TLR4), nuclear factor-κB (NF-κB), and caspase 1 were determined by real-time polymerase chain reaction and western blot analysis, respectively. The content of interleukin (IL)-1β and tumor necrosis factor-α (TNF-α) was determined by enzyme-linked immunosorbent assay. Human intestinal epithelial cell lines were induced to NEC by lipopolysaccharides (LPSs). LPS-induced cells were transfected with small interfering RNA-HMGB1 and NLRP3 plasmid vector. The mRNA and protein expression of HMGB1, NLRP3, TLR4, NF-κB, caspase 1, IL-1β, and TNF-α were determined by real-time PCR and western blot analysis, respectively.
resultsThe mRNA and protein expression of HMGB1 and NLRP3 in the NEC group was significantly higher than the control group. Inhibition of HMGB1 expression improved intestinal inflammation in newborn NEC rats. The expression of HMGB1, NLRP3, TLR4, NF-κB, and caspase 1 was upregulated in NEC and was weakened after treating with GL. LPS induction to intestinal epithelial cells markedly increased the expression of HMGB1, NLRP3, TLR4, NF-κB, caspase 1, IL-1β, and TNF-α. The knockdown of HMGB1 abolished the increase of expression, whereas further transfection with NLRP3 plasmid vector recovered the increase.
conclusionHMGB1 and NLRP3 were all upregulated in the development of NEC. Inhibition on HMGB1 could improve the intestinal inflammation in NEC by inhibiting NLRP3 via TLR4 and NF-κB signaling pathways.
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