ArticleMedical oncology (Northwood, London, England)2025
Omeprazole attenuates irradiation-induced lung injury through the suppression of apoptosis and oxidative stress in mice.
Article in Medical oncology (Northwood, London, England), 2025. 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
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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
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.
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Who cites it
1 citing paper in PubMed.
- AhR as a Common Denominator in Immunity and Inflammation in Chronic Lung Diseases: Molecular and Clinical Insights.Diseases (Basel, Switzerland) · 2026Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Radiation therapy is an effective treatment for patients with malignant thoracic tumors, but it can cause lung damage. Omeprazole (OM) is a proton pump inhibitor with anticancer, antioxidative, and anti-inflammatory activities. The aim of this study was to examine the effects of OM on oxidative stress and apoptosis through the use of ionizing radiation (IR) in lung tissue. Sixty-four mice were randomized into eight groups: the control, OM (10, 25, and 50 mg/kg/day/oral for 7 consecutive days), IR (single dose of 6 Gy), and IR + OM (10, 25, and 50 mg/kg) groups. The protective effect of OM was determined by histological and immunohistochemical evaluation and assessment of protein carbonyl levels. OM significantly decreased protein carbonyl levels in the lungs of irradiated mice compared with those in the lungs of IR-treated mice. Histological evaluation of the irradiated mice revealed destruction of the alveolar wall, thickening of the alveolar sac wall, enlarged red blood cells, infiltration of inflammatory cells, edema, and capillary, vascular and interstitial hyperemia. OM at all three doses significantly reduced lung injury. Immunohistochemical findings also revealed that OM could reduce the expression of caspase-3. OM at a low dose and short duration of administration had no side effects. OM is able to protect against lung damage caused by IR through reducing oxidative stress and decreasing the expression of caspase-3.
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Registered trials
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