ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Attenuation of chlorpyrifos-induced liver injury, oxidative stress and inflammation by selenium nanoparticles via SIRT1/FXR/Nrf2 signaling pathway modulation.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Protective effect of green tea extract on chlorpyrifos induced toxicity in liver of male mice.Scientific reports · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
The pesticide chlorpyrifos (CPF) poses significant environmental and health risks due to its toxicity. Selenium nanoparticles (Se NPs) exhibit promising therapeutic properties. This study evaluated the effects of Se NPs against CPF hepatotoxicity, focusing on oxidative and inflammatory responses, and the SIRT1/FXR/Nrf2 pathway. Rats were exposed to CPF (5.4 mg/kg body weight), with or without Se NPs (0.5 mg/kg body weight), for 28 days, followed by biochemical, histopathological, and molecular analyses. CPF administration significantly increased serum ALT and AST, reduced albumin, and induced histopathological alterations. Se NPs effectively ameliorated liver function biomarkers and mitigated histopathological changes. CPF also elevated malondialdehyde and nitric oxide, and depleted enzymatic antioxidants and GSH, which were mitigated by Se NPs. CPF upregulated NF-κB p65, TNF-α, IL-6, iNOS, Bax and caspase-3, and downregulated Bcl-2. Se NPs suppressed inflammation and apoptosis by downregulating NF-κB p65, pro-inflammatory cytokines and pro-apoptosis markers. These effects were linked to upregulation of SIRT1, FXR, Nrf2 and HO-1 and suppression of Keap1. In conclusion, Se NPs protect against CPF-induced liver injury by attenuating OS, inflammation, and apoptosis, and by upregulating SIRT1//FXR/Nrf2 signaling. These findings highlight the therapeutic potential of Se NPs in mitigating hepatotoxicity induced by exposure to CPF.
Indexed as
Identifiers
40699239What 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.