Abstract
This study is aimed at investigating the effect of amifostine (AMI) on rat bone marrow stromal stem cells (BMSCs) exposed to 2 Gy radiation. The BMSCs were divided into four groups, namely, group A that received 0 Gy radiation, group B that received 0 Gy radiation and AMI, group C that received 2 Gy radiation, and group D that received 2 Gy radiation and AMI. The proliferation, apoptosis, and distribution of BMSCs in the cell cycle, along with their osteogenesis ability, adipogenesis ability, and ROS production, were subsequently examined. The levels of ALP, PPARγ, P53, and TNFα were determined by Western blotting. The results demonstrated that the proliferation of BMSCs and the levels of ALP in group C were much lower than those in group A. The production of ROS and levels of PPARγ, P53, and TNFα in the group that received 2 Gy radiation were much higher than those in group A. Furthermore, the production of ROS and the levels of PPARγ, P53, and TNFα were much lower in group D than in group C. Additionally, the levels of ALP and extent of cell proliferation were much higher in group D than in group C. The results demonstrated the potential of AMI in reducing the side effects of radiation in BMSCs and in treatment of bone diseases caused by radiation.
Highlights
Radiotherapy (RT) is an effective strategy for the treatment of tumors, which directly kills tumor cells by inhibiting their proliferation and by inducing apoptosis [1]
Our study demonstrated that the number of apoptotic cells in the group that was exposed to 2 Gy radiation was significantly higher than that in the group that was not exposed to radiation (Figure 7)
Our study demonstrated that while radiation inhibited the osteogenic differentiation of bone marrow stromal stem cells (BMSCs), it promoted their adipogenic differentiation, which was similar to the results of the previous study [42]
Summary
Radiotherapy (RT) is an effective strategy for the treatment of tumors, which directly kills tumor cells by inhibiting their proliferation and by inducing apoptosis [1]. ROS and inflammatory cytokines induce cell cycle arrest and trigger mutagenesis, DNA damage, apoptosis, and nucleotide excision repair. These postradiation effects can lead to osteopenia and radiation-induced osteoporosis, decreasing bone strength and increasing the risk of serious fractures [4, 5]. The rate of rib fracture increases by ten times in breast cancer patients receiving radiotherapy, in comparison to normal individuals, with the incidence of fractures being as high as 22% in breast cancer patients and 24% in patients with soft tissue sarcomas [4,5,6]. Clinical data have demonstrated that the failure rate of dental implants in irradiated bones is two to three times higher than that in nonirradiated bones [8]
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