ArticleBiological research2019
CXCL8
Article in Biological research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 52 citations in OpenAlex.
- Daphnetin alleviates renal inflammation, oxidative stress, and apoptosis in septic rats via the JAK2/STAT3 signaling pathway.Histology and histopathology · 2026Article
- Targeting CXCL8 alleviates intestinal epithelial inflammation by suppressing the JAK-STAT pathway.European journal of medical research · 2025Article
- Dimethyl fumarate ameliorated pyroptosis in contrast-induced acute renal injury by regulating endoplasmic reticulum stress and JAK2-STAT3 pathway.Renal failure · 2025Article
- Regulatory effect of miR-142-5p on inflammatory process of sepsis by targeting CXCL8.Hereditas · 2025Article
- Identification of Co-Diagnostic Genes and Potential Therapeutic Targets for Asthma and Sepsis Through Mendelian Randomization and Immune Infiltration Analysis.Journal of asthma and allergy · 2025Article
- Identification of potential hub genes and drugs in septic kidney injury: a bioinformatic analysis with preliminary experimental validation.Frontiers in medicine · 2025Article
- M2 macrophage infusion ameliorates diabetic glomerulopathyRenal failure · 2024Article
- WTAP-mediated N6-methyladenosine modification promotes the inflammation, mitochondrial damage and ferroptosis of kidney tubular epithelial cells in acute kidney injury by regulating LMNB1 expression and activating NF-κB and JAK2/STAT3 pathways.Journal of bioenergetics and biomembranes · 2024Article
- Danlou tablet alleviates sepsis-induced acute lung and kidney injury by inhibiting the PARP1/HMGB1 pathway.Heliyon · 2024Article
- Article
- TRIM21 ubiquitylates GPX4 and promotes ferroptosis to aggravate ischemia/reperfusion-induced acute kidney injury.Life sciences · 2023Article
- 4-Octyl itaconate attenuates LPS-induced acute kidney injury by activating Nrf2 and inhibiting STAT3 signaling.Molecular medicine (Cambridge, Mass.) · 2023Article
- NETosis: an emerging therapeutic target in renal diseases.Frontiers in immunology · 2023Review
- Suppression of lncRNA GAS6-AS2 alleviates sepsis-related acute kidney injury through regulating the miR-136-5p/OXSR1 axisRenal failure · 2022Article
- Activation of STAT3 signaling pathway in the kidney of COVID-19 patients.Journal of nephrology · 2022Observational
- The role of CXCL8 in chronic nonhealing diabetic foot ulcers and phenotypic changes in fibroblasts: a molecular perspective.Molecular biology reports · 2022Review
- HSP70 Ameliorates Septic Acute Kidney Injury via Binding with TRAF6 to Inhibit of Inflammation-Mediated Apoptosis.Journal of inflammation research · 2022Article
- Exploring the mechanism of action of licorice in the treatment of COVID-19 through bioinformatics analysis and molecular dynamics simulation.Frontiers in pharmacology · 2022Article
- Identification of hub genes associated with acute kidney injury induced by renal ischemia-reperfusion injury in mice.Frontiers in physiology · 2022Article
- Tetrahydrocurcumin protects against sepsis-induced acute kidney injury via the SIRT1 pathway.Renal failure · 2021Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute kidney injury (AKI), which is mainly caused by sepsis, has high morbidity and mortality rates. CXCL8
methodsAn AKI mouse model was established, and kidney injury was assessed by histological analysis. The contents of serum creatinine (SCr) and blood urea nitrogen (BUN) were measured by commercial kits, whereas neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) were detected by enzyme-linked immunosorbent assay (ELISA) kits. The expressions of CXCL8 in serum and kidney tissues were determined using ELISA and immunohistochemical analysis, respectively. Apoptosis rate of renal tissue was detected by terminal deoxynucleotidyl transfer-mediated dUTP nick end labeling (TUNEL) analysis. The expressions of inflammatory cytokines were measured by quantitative real-time PCR and Western blot, respectively. The apoptosis-related proteins, JAK2, STAT3, NF-κB and IκB were determined by Western blot.
resultsG31P could reduce the levels of SCr, BUN, HGAL and KIM-1 and inhibit the renal tissue injury in AKI mice. G31P was also found to suppress the serum and nephric CXCL8 expressions and attenuated the apoptosis rate. The levels of inflammatory cytokines, pro-apoptotic proteins were decreased, while the anti-apoptotic proteins were increased by G31P in AKI mice. G31P also inhibited the activation of JAK2, STAT3 and NF-κB in AKI mice.
conclusionThese results suggest that G31P could protect renal function and attenuate the septic AKI. Our findings provide a potential target for the treatment of AKI.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.