Abstract
Selenium is considered as a trace element that plays antioxidant role in the body. So, the aim of this study was to evaluate the effect of selenium on ameliorating of sciatic nerve ischemia-reperfusion injury. Eighty (80) adult male Wistar rats weighing 250–300 g were used. They were divided into 10 groups (n = 8). Then, femoral vessels were obstructed by using 4/0 silk and splitknot techniques. After 3-h ischemia for all the groups, reperfusion was applied for different periods: 3, 7, 14, and 28 days. In half of each experimental group, 0.2 mg/kg selenium was injected intraperitoneally, coinciding with ischemia. After reperfusion, according to the grouping, rats were killed by using high dose of anesthetic drug and then sciatic nerve was removed and fixed. Then, tissue samples were processed and subsequently stained with hematoxylin-eosin, apoptosis, and immunohistochemistry stains. On the third day of reperfusion, the amount of TNF-α as an inflammatory marker of ischemia-reperfusion acute phase increased. On the seventh day of reperfusion, the amount of NF-кB as an apoptotic index and infiltration of mast cells increased in the tissue as a result of development of inflammation. But, on the 14th day of reperfusion, the amount of NF-кB as an apoptotic index decreased to the lowest amount. On the 28th day of reperfusion, the amount of TNF-α as an inflammatory marker decreased to its lowest level. Prescription of selenium concurrent with development of ischemia can reduce the damage caused by sciatic nerve ischemia-reperfusion.
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Acknowledgments
This study was approved in the Lorestan University of Medical Sciences. Special thanks to Lorestan University of Medical Sciences for the financial support, Khorramabad, Iran. The authors thank the head and staff of Razi Herbal Drugs Research Center of Lorestan Medical University.
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Zendedel, A., Gharibi, Z., Anbari, K. et al. Selenium Ameliorate Peripheral Nerve Ischemic-Reperfusion Injury via Decreased TNF-α. Biol Trace Elem Res 176, 328–337 (2017). https://doi.org/10.1007/s12011-016-0836-7
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DOI: https://doi.org/10.1007/s12011-016-0836-7