ArticleHeliyon2024
The protective effects of selenium and boron on cyclophosphamide-induced hepatic oxidative stress, inflammation, and apoptosis in rats.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
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Who cites it
6 citing papers in PubMed.
- Atorvastatin Reduces Alcohol-Related Cardiac and Liver Tissue Damage, Oxidative Stress, Inflammation, Apoptosis, and Thiol-Disulfide Imbalance in Rats.Journal of biochemical and molecular toxicology · 2026Article
- Metabolomics and Network Pharmacology-Based Screening of Candidate Hepatoprotective Metabolites in FermentedCurrent issues in molecular biology · 2026Article
- Investigation of Prophylactic and Therapeutic Effects of Boric Acid in an Experimental Mechanical Biliary Obstructive Cholestasis Rat Model.Biological trace element research · 2026Article
- Boron Prevents Oral Acrylamide Damage in Bone Marrow and Hematologic Parameters of Wistar Rats.Biological trace element research · 2025Article
- Isorhamnetin: Reviewing Recent Developments in Anticancer Mechanisms and Nanoformulation-Driven Delivery.International journal of molecular sciences · 2025Review
- Protective Effect of Escin Against Kidney Injury: Histopathological and Biochemical Evaluations.Current issues in molecular biology · 2024Article
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cyclophosphamide (CP) is an alkylating anticancer drug with broad clinical application that is highly effective in the treatment of cancer and non-malignant diseases. However, the main limiting effect of CP is multi-organ toxicity due to damage to normal tissues. The aim of this study is to compare the hepatoprotective potential of selenium (Se) and boron (B) in CP-induced liver injury in experimental rats. The rats were randomly divided into six equal groups: Control (saline), 200 mg/kg CP (administered once on the fourth day of the experiment), 1.5 mg/kg Se (administered once/time daily for 6 days), 20 mg/kg B (administered once/time daily for 6 days), Se + CP and B + CP administered intraperitoneally (i.p.). Administration of CP leads to an increase in the levels of apoptotic markers (Bax, caspase-3), the apoptotic signaling pathway (Nrf2), oxidative stress indicators (TOS, OSI), lipid peroxidation markers (MPO, MDA), inflammation levels (NF-kB, TNF-α, IL-1β, IL -6), liver function markers (ALT, AST, ALP), while apoptosis markers (Bcl-2), apoptosis pathway (Keap-1), oxidative stress indicator (TAS), inflammation (IL -10) and intracellular antioxidant defense system (SOD, CAT, GPx and GSH) decreased. In addition, degeneration of hepatocytes and congestion in the central veins were observed. In contrast, in the groups administered Se and B with CP, the changes that occurred were reversed. However, it was found that Se protects the liver slightly better against CP damage than B. The protective effect of Se and B against the toxic effects of CP on the antioxidant markers SOD, CAT and GPx1 was also investigated
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