ArticleFrontiers in pharmacology2025
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Structural dynamics, pathogenic mechanisms, and therapeutic targeting of the NLRP3 inflammasome in lupus nephritis.Frontiers in immunology · 2026Review
- Study on the pro-inflammatory injury of neutrophil extracellular traps in gouty nephropathy.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aim: The aim of this study was to investigate whether Methods: The HRI rat model was established using a hypobaric hypoxia chamber. Rats were divided into a control group, a hypoxia group, low-dose ABPS (ABPL) group, a high-dose ABPS (ABPH) group, a DNase I-positive control group, and an NLRP3 agonist nigericin sodium salt (NSS) group. Blood serum components relevant to neutrophil extracellular traps (NETs), including cell-free DNA (cf-DNA), myeloperoxidase-DNA (MPO-DNA), neutrophil elastase-DNA (NE-DNA), citrullinated histone 3 (cit-H3), blood urea nitrogen (BUN), serum creatinine (Scr), cystatin C (CysC), neutrophil gelatinase-associated lipocalin (NGAL), and kidney injury molecule-1 (KIM-1), were analyzed. NOD-like receptor protein 3 (NLRP3) pathway proteins, MPO, NE, cit-H3, and reactive oxygen species (ROS) in renal tissues were analyzed by multiplex fluorescence immunohistochemistry. MPO and cit-H3 in renal tissues were analyzed via Western blot. Oxidative stress markers such as malondialdehyde (MDA) and superoxide dismutase (SOD) were analyzed using the thiobarbituric acid (TBA) assay. Results: The results demonstrated that ABPSs exerted protective effects against hypoxic renal injury. First, ABPSs significantly reduced the levels of cf-DNA, MPO-DNA, and cit-H3, with efficacy comparable to that of DNase I. Second, ABPSs markedly suppressed the activation of the NLRP3 inflammasome pathway by degrading NETs, as evidenced by reduced protein expression of NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), and caspase-1, accompanied by significant decreases in interleukin 1β (IL-1β) and IL-18. Furthermore, ABPSs effectively alleviated oxidative stress by reducing MDA, enhancing SOD activity, and attenuating ROS. Finally, these molecular and cellular improvements translated into functional recovery as high-dose ABPS treatment restored renal function to near-normal levels, including a 58.1% reduction in BUN, a 34.5% reduction in Scr, a 23.6% reduction in NGAL, a 29.6% reduction in KIM-1, and a 32.2% reduction in CysC. Hematoxylin and eosin (H&E) and periodic acid-Schiff (PAS) staining and quantitative scoring analysis of kidney injury revealed severe tubular necrosis and glomerular damage in rats in the hypoxia group, which were significantly attenuated in both the ABPL and ABPH groups ( Conclusion: ABPS mitigates hypoxic renal injury by reducing NETs and synergistically regulating oxidative stress. ABPS shows potential as a multi-target, low-toxicity candidate for renal protection.
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Registered trials
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