51. Protective Effect of JXT Ethanol Extract on Radiation-Induced Hematopoietic Alteration and Oxidative Stress in the Liver
- Author
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Xian-Zhe Dong, Xiao Tan, Dai-Hong Guo, Ping Liu, Yu-Ning Wang, and Can Yan
- Subjects
0301 basic medicine ,Aging ,Article Subject ,Protective Agents ,medicine.disease_cause ,Biochemistry ,Antioxidants ,Superoxide dismutase ,Andrology ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,medicine ,Humans ,Viability assay ,lcsh:QH573-671 ,Ipomoea batatas ,Cells, Cultured ,chemistry.chemical_classification ,Reactive oxygen species ,biology ,lcsh:Cytology ,Plant Extracts ,Glutathione peroxidase ,Cell Biology ,General Medicine ,Malondialdehyde ,Plant Leaves ,Oxidative Stress ,030104 developmental biology ,medicine.anatomical_structure ,Liver ,chemistry ,Gamma Rays ,030220 oncology & carcinogenesis ,Toxicity ,biology.protein ,Bone marrow ,Reactive Oxygen Species ,Oxidative stress ,Research Article - Abstract
This study aims at investigating the radioprotective effect of ethanol extract from Ji-Xue-Teng (JXT,Spatholobus suberectus) on radiation-induced hematopoietic alteration and oxidative stress in the liver. Mice were exposed to a single acuteγ-radiation for the whole body at the dose of 6.0 Gy, then subjected to administration of amifostine (45 mg/kg) or JXT (40 g crude drug/kg) once a day for 28 consecutive days, respectively. Bone marrow cells and hemogram including white cells, red cells, platelet counts, and hemoglobin level were examined. The protein expression levels of pJAK2/JAK2, pSTAT5a/STAT5a, pSTAT5b/STAT5b, and Bcl-2 in bone marrow tissue; levels of reactive oxygen species (ROS); and the activity of superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GSH-Px) in serum and liver tissue were determined. At the end of the experiment, the effect of JXT on cell viability and G-CSF and G-CSFR levels in NFS-60 cells were tested by CCK-8 assay, ELISA, and flow cytometry. The results showed that the mice exposed toγ-radiation alone exhibited a typical hematopoietic syndrome. In contrast, at the end of the 28-day experiment, irradiated mice subjected to oral administration of JXT showed an obvious improvement on blood profile with reduced leucopenia, thrombocytopenia (platelet counts), RBC, and hemoglobin levels, as well as bone marrow cells. The expression of pJAK2/JAK2, pSTAT5a/STAT5a, and Bcl-2 in bone marrow tissue was increased after JXT treatment. The elevation of ROS was due to radiation-induced toxicity, but JXT significantly reduced the ROS level in serum and liver tissue, elevated endogenous SOD and GSH-PX levels, and reduced the MDA level in the liver. JXT could also increase cell viability and G-CSFR level in NFS-60 cells, which was similar to exogenous G-CSF. Our findings suggested that oral administration of JXT effectively facilitated the recovery of hematopoietic bone marrow damage and oxidative stress of the mice induced byγ-radiation.
- Published
- 2018
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