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<p>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.</p>

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Omeprazole attenuates irradiation-induced lung injury through the suppression of apoptosis and oxidative stress in mice

  • 期刊论文

  • 发表日期：

    2025年4月22日

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  • Fereshteh Talebpour Amiri,
  • Mohammad Asghari,
  • Seyed Jalal Hosseinimehr

摘要

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.