ArticleReports of biochemistry & molecular biology2024
Celastrol Mitigates Acetaminophen-Induced Nephrotoxicity in Rats via Targeting Renal Oxidative Stress, Inflammation, Apoptosis with Enhancement in Aquaporin 1 Level.
Article in Reports of biochemistry & molecular biology, 2024. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Paracetamol Induces Apoptosis, Reduces Colony Formation, and Increases PTPRO Gene Expression in Human Embryonic Kidney HEK 293 Cells.Journal of biochemical and molecular toxicology · 2025Article
- Nrf2-mediated mechanistic pathways of celastrol nephroprotection: disrupting the oxidative-inflammatory-apoptotic axis in cypermethrin toxicity.Frontiers in pharmacology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Acetaminophen also name paracetamol is apopular antipyretic and analgesic drug, in alarge doses produces a cute kidney injury either in human and animals. The aim of this study to assess the effect of celastrol in reducing acetaminophen-induced nephrotoxicity and to elucidate its underlying mechanisms. Methods: Rats were divided into four groups: control, celastrol-treated, acetaminophen-exposed, and a group receiving both acetaminophen and celastrol. After 24 hours, blood samples were taken and kidney tissues were harvested for histological and molecular analyses. The findings shed light on the protective effects of celastrol against acetaminophen-induced nephrotoxicity, offering insights into its therapeutic potential. Results: paracetamol oral intake altered renal histology with significantly P< 0.05 increased serum creatinine, blood urea nitrogen (BUN), and homogenate malonaldhyde (MDA), and immunoexpression of tumor necrosis- alpha (TNF-α), interleukin-6 (IL-6), caspase-3, Bcl-2-associated X- protein (Bax). Furthermore, it decreases homogenate level of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and gene expression of nuclear factor erythroid 2-related factor 2 (Nrf2), and haem oxygenase-1 (HO-1). Meanwhile, intraperitoneal injection of celastrol with acetaminophen reaffirms the previous results. Conclusions: We provided a novel treatment against acetaminophen induced-nephrotoxicity with targeting renal oxidative stress, inflammation, apoptosis with elevation of Aquaporin 1 (AQP1) level.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.