Objective: We investigated the effects of bumetanide alone and in combination with dexamethasone on facial nerve regeneration in rats with facial paralysis.
Study Design: A prospective controlled animal study.
Setting: An animal laboratory.
Subjects And Methods: Facial paralysis was induced in 32 Wistar rats that we then divided into 4 groups: group 1, control; group 2, bumetanide; group 3, dexamethasone; group 4, bumetanide and dexamethasone. Electroneurography was performed 1, 2, and 4 weeks later, and nerve regeneration was evaluated by electron and light microscopy and Western blotting in week 4.
Results: Regarding the comparison between preoperative values and week 4, the latency difference in group 1 (1.25 milliseconds) was significantly higher than those of groups 2 to 4 (0.56, 0.34, and 0.10 milliseconds, respectively; = .001). The latency increment in groups 2 and 3 was higher than that of group 4 ( = .002 and = .046) in week 4, whereas groups 2 and 3 did not differ significantly ( = .291). Amplitude difference was not statistically significant from week 4 among all groups (all .05). The number of myelinated axons was significantly higher in all treatment groups than in the control group ( = .001). Axon number and intensity were significantly higher in group 4 as compared with groups 2 and 3 ( = .009, = .005).
Conclusion: After primary neurorrhaphy, dexamethasone and bumetanide alone promoted nerve recovery based on electrophysiologic and histologic measures. Combination therapy was, however, superior.
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http://dx.doi.org/10.1177/0194599820937670 | DOI Listing |
ACS Omega
December 2024
School of Physical Sciences and Nanotechnology, Yachay Tech University, Urcuquí 100119, Ecuador.
Samarium-doped nanohydroxyapatite is a biomaterial with nerve regeneration activity and bioimaging. In this work, Sm/HAp; (Ca Sm (PO)(OH)) (0 ≤ ≤ 1) was synthesized using the hydrothermal method and thermally treated from 200 to 800 °C. The samples were characterized by transmission electron microscopy, energy-dispersive X-ray spectroscopy, Fourier transform infrared spectroscopy, X-ray diffraction, Raman spectroscopy, and luminescence spectroscopy.
View Article and Find Full Text PDFExploration (Beijing)
December 2024
ATP synthase inhibitory factor 1 (ATPIF1), a key modulator of ATP synthase complex activity, has been implicated in various physiological and pathological processes. While its role is established in conditions such as hypoxia, ischemia-reperfusion injury, apoptosis, and cancer, its involvement remains elusive in peripheral nerve regeneration. Leveraging ATPIF1 knockout transgenic mice, this study reveals that the absence of ATPIF1 impedes neural structural reconstruction, leading to delayed sensory and functional recovery.
View Article and Find Full Text PDFFront Cell Dev Biol
December 2024
Department of Ophthalmology, Tufts Medical Center, Tufts University School of Medicine, Boston, MA, United States.
The cornea is densely innervated to maintain the integrity of the ocular surface, facilitating functions such as sensation and tear production. Following damage, alterations in the corneal microenvironment can profoundly affect its innervation, potentially impairing healing and sensory perception. One protein frequently upregulated at the ocular surface following tissue damage is galectin-3, but its contribution to corneal nerve regeneration remains unclear.
View Article and Find Full Text PDFFront Neurosci
December 2024
Department of Otorhinolaryngology and Head and Neck Surgery, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Background And Aim: The administration of growth and neurotrophic factors has been attempted experimentally as a new therapeutic strategy for severe facial paralysis. Granulocyte colony-stimulating factor (G-CSF) has an effect on the treatment of central nervous system injuries, such as cerebral infarction and spinal cord injury. This study aimed at examining the effects of G-CSF on facial nerve regeneration in rats.
View Article and Find Full Text PDFCell Regen
December 2024
Department of Neurology, Affiliated Hospital of Jining Medical University, 89 Guhuai Road, Jining, 272029, Shandong Province, China.
Peripheral nerve injury (PNI) usually causes severe motor, sensory and autonomic dysfunction. In addition to direct surgical repair, rehabilitation exercises, and traditional physical stimuli, for example, electrical stimulation, have been applied in promoting the clinical recovery of PNI for a long time but showed low efficiency. Recently, significant progress has been made in new physical modulation to promote peripheral nerve regeneration.
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