ArticleSaudi journal of biological sciences2020
The role of activated NLRP3 inflammatory body in acute kidney injury in rats caused by sepsis and NLRP3-TXNIP signaling pathway.
Article in Saudi journal of biological sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- The LncRNA MIAT acts as a sponge for miR-942-5p to exacerbate the inflammation and oxidative stress in macrophages during sepsis-associated liver injury.BMC immunology · 2026Article
- Cuproptosis-related gene TMPO affects the healing of diabetic foot ulcers through TGF-β/Smad signaling pathway.iScience · 2025Article
- Association between serum uric acid to albumin ratio and all-cause mortality in critically ill patients with sepsis: a retrospective study.BMC infectious diseases · 2025Article
- Zhike Erfang Alleviates MRSA-Induced Pneumonia by Inhibiting TRAF6 and Activating NLRP3 Inflammatory Body.Journal of inflammation research · 2025Article
- Novel insights into NOD-like receptors in renal diseases.Acta pharmacologica Sinica · 2022Review
- Malvidin alleviates mitochondrial dysfunction and ROS accumulation through activating AMPK-α/UCP2 axis, thereby resisting inflammation and apoptosis in SAE mice.Frontiers in pharmacology · 2022Article
- The NLRP3 Inflammasome Inhibitor Dapansutrile Attenuates Cyclophosphamide-Induced Interstitial Cystitis.Frontiers in immunology · 2022Article
- Molecular mechanisms and functions of pyroptosis in sepsis and sepsis-associated organ dysfunction.Frontiers in cellular and infection microbiology · 2022Review
- KCNQ1OT1 Influences HK-2 Apoptosis and Inflammation in LPS-Induced Acute Renal Injury via Modulating miR-30a-5p/NLRP3 Axis.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Long non-coding RNA NEAT1 promotes lipopolysaccharide-induced injury in human tubule epithelial cells by regulating miR-93-5p/TXNIP axis.Medical microbiology and immunology · 2021Article
- Tranilast: a potential anti-Inflammatory and NLRP3 inflammasome inhibitor drug for COVID-19.Immunopharmacology and immunotoxicology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe model of acute renal injury (AKI) induced by sepsis in rats was established by abdominal resection through surgical suture. The activation mechanism of nod-like receptor with pyrin domain containing 3 (NLRP3) inflammatory corpuscle in AKI induced by sepsis was analyzed.
methodsHere, 60 male rats were selected and divided into two groups, including sham-operated group (NO-OPs group, n = 15) and sepsis group (CELP group, n = 45). In order to examine each index of CELP group, four time points (10, 20, 30, and 40 h) were set as control. In NO-OPs group, only abdominal resection through surgical suture was carried out. The expression levels of NLRP3, apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain (ASC), caspase-1, and the expression level of NLRP3-TXNIP signaling pathway were measured by immunohistochemistry, Western blotting, immunoprecipitation, and mito-TEMPO (a mitochondria-targeted antioxidant) 40 h after operation and 10, 20, 30, and 40 h post-operation in CELP group. Herein, 40 h post-operation in NO-OPs group and 10, 20, 30, and 40 h post-operation in CELP group, peripheral blood samples were collected.
resultsCompared with NO-OPs group, the levels of serum creatinine (Scr) and blood urea nitrogen (BUN) in CELP group were increased (P < 0.05). Compared with NO-OPs group, the expression levels of interleukin-1β (IL-1β), NLRP3, ASC, and caspase-1 in CELP group were increased (P < 0.05). The expression level of TXNIP in renal tubular epithelial cells in rats was up-regulated. There was a positive correlation between TXNIP and NLRP3. The binding of NLRP3-TXNIP signaling pathway could be inhibited by siRNA transfection or mito-TMPO, and the activity of NLRP3 inflammatory bodies could be inhibited as well.
conclusionActivation of NLRP3 inflammatory corpuscles could promote AKI induced by sepsis. Simultaneously, renal injury may lead to the production of mitochondrial reactive oxygen species (mROS), which may induce the binding of TXNIP to NLRP3.
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