Fooladi Masoomeh, Cheki Mohsen, Shirazi Alireza, Sheikhzadeh Peyman, Amirrashedi Mahsa, Ghahramani Fatemeh, Khoobi Mehdi
PhD Candidate, Department of Medical Physics and Biomedical Engineering, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
PhD, Department of Medical Imaging and Radiation Sciences, Faculty of Paramedicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
J Biomed Phys Eng. 2022 Jun 1;12(3):277-284. doi: 10.31661/jbpe.v0i0.2012-1243. eCollection 2022 Jun.
Radiation-induced hematopoietic suppression and myelotoxicity can occur due to the nuclear accidents, occupational irradiation and therapeutic interventions. Bone marrow dysfunction has always been one of the most important causes of morbidity and mortality after ionizing irradiation.
This study aims to investigate the protective effect of telmisartan against radiation-induced bone marrow injuries in a Balb/c mouse model.
In this experimental study, male Balb/c mice were divided into four groups as follow: group 1: mice received phosphate buffered saline (PBS) without irradiation, group 2: mice received a solution of telmisartan in PBS without irradiation, group 3: mice received PBS with irradiation, and group 4: mice received a solution of telmisartan in PBS with irradiation. A solution of telmisartan was prepared and administered orally at 12 mg/kg body weight for seven consecutive days prior to whole body exposing to a single sub-lethal dose of 5 Gy X-rays. Protection of bone marrow against radiation induced damage was investigated by Hematoxylin-Eosin (HE) staining assay at 3, 9, 15 and 30 days after irradiation.
Histopathological analysis indicated that administration of telmisartan reduced X-radiation-induced damage and improved bone marrow histology. The number of different cell types in bone marrow, including polymorphonuclear /mononuclear cells and megakaryocytes significantly increased in telmisartan treated group compared to the only irradiated group at all-time points.
The results of the present study demonstrated an efficient radioprotective effect of telmisartan in mouse bone marrow against sub-lethal X-irradiation.
核事故、职业辐射和治疗干预可能导致辐射诱导的造血抑制和骨髓毒性。骨髓功能障碍一直是电离辐射后发病和死亡的最重要原因之一。
本研究旨在探讨替米沙坦对Balb/c小鼠模型辐射诱导的骨髓损伤的保护作用。
在本实验研究中，雄性Balb/c小鼠分为四组，如下：第1组：小鼠接受未照射的磷酸盐缓冲盐水（PBS）；第2组：小鼠接受未照射的PBS中替米沙坦溶液；第3组：小鼠接受照射的PBS；第4组：小鼠接受照射的PBS中替米沙坦溶液。制备替米沙坦溶液，并在全身暴露于单次亚致死剂量5 Gy X射线前，以12 mg/kg体重口服给药，连续7天。在照射后3、9、15和30天，通过苏木精-伊红（HE）染色分析研究骨髓对辐射诱导损伤的保护作用。
组织病理学分析表明，替米沙坦给药减少了X射线辐射诱导的损伤，并改善了骨髓组织学。在所有时间点，与仅照射组相比，替米沙坦治疗组骨髓中不同细胞类型的数量，包括多形核/单核细胞和巨核细胞显著增加。
本研究结果表明，替米沙坦对小鼠骨髓亚致死性X射线辐射具有有效的辐射防护作用。
