Effects of Selenium on Axon and Myelin Healing in an Experimental Sciatic Nerve Injury Model

Abstract

Objective: Although, the neuroprotective effects of selenium are known, its effect on peripheral nerve injury is not clear. The study was aimed to investigate whether selenium prevents axonal and myelin damage in experimental sciatic nerve injury. Materials and Methods: Twenty-eight male Wistar albino rats were divided into four groups (n=7 in each): control (C), selenium (S), injury (I), and selenium-treated injury (SI). Injury was generated by 30 second of compression via Yasargil aneurysm clip on the sciatic nerve of rats in the I and SI groups. Then, selenium was given to the S and SI groups as 1.5 mg/ kg by oral gavage at 1 st , 24 th , 48 th and 72 nd hour after surgery. According to the experimental protocol, electrophysiological, histological, and biochemical tests were performed end of the day 4. Results: Whereas the amplitude of compound action potential, nerve conduction velocity, average axon diameter, myelin thickness, myelinated/unmyelinated axons and SOD activity in red blood cells of the I group were significantly lower than those of the C, S and SI groups, the serum MDA levels of the I group were significantly higher than those of the C, S and SI groups. Conclusion:The findings of this study show that selenium decreases axonal and myelin damage after sciatic nerve injury and that this neuroprotective effect of selenium is at least partially mediated by oxidant/antioxidant mechanisms.

The SELENOT mimetic PSELT promotes nerve regeneration by increasing axonal myelination in a facial nerve injury model in female rats

“…These changes in neural cells promote ROS formation (Llobet Rosell & Neukomm, 2019; Rodella et al, 2016), which is reduced by various antioxidant molecules whose expression is stimulated in motor neurons as demonstrated for glutathione reductase, thioredoxin 1, and the selenoprotein thioredoxin reductase 1 in a hypoglossal nerve injury model in rats (Hama et al, 2010; Mansur et al, 1998). In fact, PSELT may balance ROS and nitric oxide levels to maintain them at sustainable levels for SC, thus enabling these cells to release neurotrophic factors necessary for the regeneration of the injured nerve, as previously suggested also for selenium or ascorbic acid (Huff et al, 2020; Kizilay et al, 2017). This potential pro‐survival antioxidant effect of PSELT could be carried by the trace element selenium present in PSELT, which was recently shown to exert a protective effect against ferroptosis in neural tissue (Alim et al, 2019; Ingold et al, 2018).…”

The Role of Dietary Nutrients in Peripheral Nerve Regeneration

“…It has been shown that selenium administration improved nerve regeneration after nerve compression in terms of electrophysiological and histological results (higher axon diameter, myelin thickness, and myelinated axon numbers) compared to untreated animals. The authors speculated that the preventive effects of selenium on axons and myelin could be mediated through blockage or reduction of the effects of lipid peroxidation chain reactions or through a positive effect on SCs due to a decrease in the effect of oxidative stress [166].…”