ArticleNaunyn-Schmiedeberg's archives of pharmacology2024
MitoQ and its hyaluronic acid-based nanopreparation mitigating gamma radiation-induced intestinal injury in mice: alleviation of oxidative stress and apoptosis.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 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.
- Protective mechanisms and therapeutic promise of nanomaterials in radiation-induced diseases.International journal of pharmaceutics: X · 2026Review
- Unraveling the molecular landscape of chronic radiation injury: From oxidative stress signaling to translational modeling (Review).International journal of molecular medicine · 2026Review
- Piceatannol ameliorates intestinal barrier dysfunction in urosepsis by modulating the Nrf2/ROS/NF-κB pathway.Scientific reports · 2026Article
- The radioprotective effect of olanzapine on intestinal injury via modulation of oxidative stress, NF-κB, and caspase-3 expression.Journal of molecular histology · 2026Article
- MitoQ alleviates malathion‑induced hepatorenal toxicity via oxidative stress and inflammation modulation.Molecular medicine reports · 2025Article
- Mitochondria-targeted antioxidant MitoQ radiosensitizes tumors by decreasing mitochondrial oxygen consumption.Cell death discovery · 2024Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Perturbations produced by ionizing radiation on intestinal tissue are considered one of highly drastic challenges in radiotherapy. Animals were randomized into five groups. The first group was allocated as control, and the second was subjected to whole body γ-irradiation (10 Gy). The third was administered HA NP (17.6 mg/kg/day; i.p.) and then irradiated. The fourth one received MitoQ (2 mg/kg/day; i.p.) and then irradiated. The last group received MitoQ/HA NP (2 mg/kg/day; i.p.) for 5 days prior to irradiation. Mice were sacrificed a week post-γ-irradiation for evaluation. MitoQ/HA NP ameliorated mitochondrial oxidative stress as indicated by rising (TAC) and glutathione peroxidase and decreasing malondialdehyde, showing its distinguished antioxidant yield. That impacted the attenuation of apoptosis, which was revealed by the restoration of the anti-apoptotic marker and lessening proapoptotic caspase-3. Inflammatory parameters dwindled via treatment with MitoQ/HA NP. Moreover, this new NP exerts its therapeutic action through a distinguished radioprotective pathway (Hmgb1/TLR-4.) Subsequently, these antioxidants and their nanoparticles conferred protection to intestinal tissue as manifested by histopathological examination. These findings would be associated with its eminent antioxidant potential through high mitochondria targeting, enhanced cellular uptake, and ROS scavenging. This research underlines MitoQ/HA NP as a new treatment for the modulation of intestinal damage caused by radiotherapy modalities.
Indexed as
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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 OpenQuestion graph.