Ternary magnesium alloys with low combined addition of elements gadolinium and zinc were developed in the present work, with their microstructures, mechanical properties, in vitro degradation behaviors, and cytotoxicity being systematically studied. Furthermore, the Mg-1.8Zn-0.2Gd alloy, with the best in vitro performance, was implanted into Sprague Dawley rats to examine its in vivo degradation performance for up to 6 months. It was found that Mg-1.8Zn-0.2Gd, composed of a single α-Mg phase, owned excellent strength and toughness that were comparable to the CE marked MAGNEZIX, the mischmetal added Mg alloy. Owing to the uniform single-phased microstructure, the degradation rate of this alloy was around 0.12 mm/y measured by electrochemical testing, which was comparable to high purity magnesium. Moreover, the Mg-1.8Zn-0.2Gd alloy exhibited no cytotoxicity to L929, MG63, and VSMC cells. In vivo degradation characterized by micro-computed tomography revealed that the Mg-1.8Zn-0.2Gd implant could maintain structural integrity in the first 2 months, and serious degradation could be observed after 6 months. A remarkable 100% survival rate of experimental animals was observed with no negative effects on bone tissues. The implant and the surrounding bone were well integrated within 2 months, implying good biocompatibility and osteoconductivity of the experimental alloy. On the basis of the above findings, the feasibility of Mg-Zn-Gd alloys for use as orthopedic implants was systematically discussed. This study provides a new strategy for development of high-performance Mg-rare earth (RE)-based alloys with superior mechanical properties and corrosion resistance while effectively avoiding the possible standing toxic effect of RE elements.
BackgroundElectrical stimulation (ES) has been proven to be an effective means of enhancing the speed and accuracy of nerve regeneration. However, these results were recorded when the procedure was performed almost immediately after nerve injury. In clinical settings, most patients cannot be treated immediately. Some patients with serious trauma or contaminated wounds need to wait for nerve repair surgery. Delays in nerve repair have been shown to be associated with poorer results than immediate surgery. It is not clear whether electrical stimulation still has any effect on nerve regeneration after enough time has elapsed.MethodsA delayed nerve repair model in which the rats received delayed nerve repair after 1 day, 1 week, 1 month, and 2 months was designed. At each point in time, the nerve stumps of half the rats were bridged with an absorbable conduit and the rats were given 1 h of weak electrical stimulation. The other half was not treated. In order to analyze the morphological and molecular differences among these groups, 6 ES rats and 6 sham ES rats per point in time were killed 5 days after surgery. The other rats in each group were allowed to recover for 6 weeks before the final functional test and tissue observation.ResultsThe amounts of myelinated fibers in the distal nerve stumps decreased as the delay in repair increased for both ES rats and sham ES rats. In the 1-day-delay and 1-week-delay groups, there were more fibers in ES rats than in sham ES rats. And the compound muscle action potential (CMAP) and motor nerve conduction velocity (MNCV) results were better for ES rats in these two groups. In order to analyze the mechanisms underlying these differences, Masson staining was performed on the distal nerves and quantitative PCR on the spinal cords. Results showed that, after delays in repair of 1 month and 2 months, there was more collagen tissue hyperplasia in the distal nerve in all rats. The brain-derived neurotrophic factor (BDNF) and trkB expression levels in the spinal cords of ES rats were higher than in sham ES rats. However, these differences decreased as the delay in repair increased.ConclusionsElectrical stimulation does not continue to promote nerve regeneration after long delays in nerve repair. The effective interval for nerve regeneration after delayed repair was found to be less than 1 month. The mechanism seemed to be related to the expression of nerve growth factors and regeneration environment in the distal nerves.
rGO-based conductive nerve conduit as a scaffold to bridge peripheral nerve transected injury and 2 mm gap provides a suitable microenvironment for axons selective regeneration.
Our previous study showed that systemic administration of the traditional Chinese medicine Epimedium extract promotes peripheral nerve regeneration. Here, we sought to explore the therapeutic effects of local administration of icariin, a major component of Epimedium extract, on peripheral nerve regeneration. A poly(lactic-co-glycolic acid) biological conduit sleeve was used to bridge a 5 mm right sciatic nerve defect in rats, and physiological saline, nerve growth factor, icariin suspension, or nerve growth factor-releasing microsphere suspension was injected into the defect. Twelve weeks later, sciatic nerve conduction velocity and the number of myelinated fibers were notably greater in the rats treated with icariin suspension or nerve growth factor-releasing microspheres than those that had received nerve growth factor or physiological saline. The effects of icariin suspension were similar to those of nerve growth factor-releasing microspheres. These data suggest that icariin acts as a nerve growth factor-releasing agent, and indicate that local application of icariin after spinal injury can promote peripheral nerve regeneration.
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