ArticleMolecular biology reports2024
Histone deacetylase inhibitor, Trichostatin A mitigates ionizing radiation induced redox imbalance by regulating NRF2/GPX4/PINK1/PARKIN signaling in mice intestine.
Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Review
- How histone modifications influence cellular radiosensitivity: Pharmaceutically targeting epigenetic regulators as a promising avenue to overcome radioresistance.Acta pharmaceutica Sinica. B · 2025Review
- Radiation-induced intestinal injury: from molecular mechanisms to clinical translation.Oncology reviews · 2025Review
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Authors and funding
4 authors.
Funding
Abstract
backgroundGastrointestinal-acute radiation syndrome (GI-ARS) caused by moderate to high doses of ionizing radiation exposure contribute to early death in humans. GI injury is also a common adverse effect seen in cancer patients undergoing abdominal/pelvic radiotherapy. Currently, no countermeasure agents have been approved for medical management of GI-ARS. The present study aims to evaluate the mechanism of action of Trichostatin A(TSA), a pan histone deacetylase inhibitor, against radiation-induced GI injury.
methodsTSA (150 ng/kg bw) was administered to mice 1 h and 24 h after 15 Gy abdominal irradiation. Expression of various markers of oxidative stress, mitochondrial dysfunction, and apoptosis were checked in the jejunum, and their possible regulation through the Nrf2 signaling pathway was evaluated.
resultsTSA administered post-irradiation (15 Gy + TSA) elevated intestinal total antioxidant and glutathione levels by regulating the expression of Slc7A11 and antioxidant proteins, GCLC, GPX4, and TXNRD1. Improved mitochondrial membrane potential, ATP levels, downregulation of mitochondrial quality control proteins, (PINK1 and PARKIN), and differential regulation of the apoptotic proteins, (BAX, PUMA and BCL2) with reduced intestinal epithelial cell apoptosis in the TSA-adminstered group were observed. TSA also upregulated Nrf2 in the presence of its specific inhibitor, ML385, suggesting its involvement in regulating Nrf2 signaling during oxidative stress induced by radiation in intestine. H & E stained jejunum cross-sections revealed that TSA mitigated radiation-mediated intestinal injury in mice.
conclusionsPresent findings indicate that TSA is beneficial in mitigating the damaging effects of ionizing radiation in the intestine.
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