Objectives: In this study, the impact of thiamine (Thi), N-acetyl cysteine (NAC), and dexamethasone (DEX) were investigated in axotomized rats, as a model for neural injury.
Materials And Methods: Sixty-five axotomized rats were divided into two different experimental approaches, the first experiments included five study groups (n=5): intrathecal Thi (Thi.it), intraperitoneal (Thi), NAC, DEX, and control. Cell survival was assessed in L5DRG in the 4 week by histological assessment. In the second study, 40 animals were engaged to assess , , , and expression in L4-L5DRG in the 1 and 2 weeks after sural nerve axotomy under treatment of these agents (n=10).
Results: Ghost cells were observed in morphological assessment of L5DRG sections, and following stereological analysis, the volume and neuronal cell counts significantly were improved in the NAC and Thi.it groups in the 4 week (<0.05). Although expression did not show significant differences, was reduced in the Thi group (=0.01); and the ratio increased in the NAC group (1 week, <0.01). Furthermore, the and expression decreased in the Thi and NAC groups, on the 1 week of treatment (≤0.05 and <0.01). However, in the 2 week, the expression in both Thi and NAC groups (<0.01), and the expression in the DEX group (=0.05) were significantly decreased.
Conclusion: The findings may classify Thi in the category of peripheral neuroprotective agents, in combination with routine medications. Furthermore, it had strong cell survival effects as it could interfere with the destructive effects of by increasing .
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http://dx.doi.org/10.22038/IJBMS.2023.67157.14726 | DOI Listing |
Int J Mol Sci
November 2024
Department of Physiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Rd., Wuhan,430030, China.
In vitro experiments performed on dissociated dorsal root ganglion (DRG) neurons suggest the involvement of the hyperpolarization-activated cation current (I) in enhancing neuronal excitability, potentially contributing to neuropathic pain. However, the more confirmative in vivo information about how nerve injury interacts with I is lacking. In this study, I was recorded in vivo using the dynamic single-electrode voltage clamp (dSEVC) technique on L5 DRG neurons of normal rats and those seven days after spinal nerve axotomy (SNA).
View Article and Find Full Text PDFBiology (Basel)
November 2024
Laboratory of Nerve Regeneration, University of Campinas (UNICAMP), Campinas 13083-865, SP, Brazil.
Spinal cord injury results in significant motor and sensory loss. In the experimental ventral root avulsion (VRA) model, the ventral (motor) roots are disconnected from the spinal cord surface, disrupting contact between spinal motoneurons and muscle fibers. Axotomized motoneurons typically degenerate within two to three weeks after avulsion, the situation being exacerbated by an increased glial response and chronic inflammation.
View Article and Find Full Text PDFCell Death Discov
June 2024
North Texas Eye Research Institute, School of Biomedical Sciences, University of North Texas Health Science Center, Fort Worth, TX, USA.
This study assesses the neuroprotective potential of CPP-P1, a conjugate of an anti-apoptotic peptain-1 (P1) and a cell-penetrating peptide (CPP) in in vitro, in vivo, and ex vivo glaucoma models. Primary retinal ganglion cells (RGCs) were subjected to either neurotrophic factor (NF) deprivation for 48 h or endothelin-3 (ET-3) treatment for 24 h and received either CPP-P1 or vehicle. RGC survival was analyzed using a Live/Dead assay.
View Article and Find Full Text PDFStem Cell Res Ther
March 2024
Department of Structural and Functional Biology, Laboratory of Nerve Regeneration, Institute of Biology, University of Campinas, Campinas, 13083-862, SP, Brazil.
Background: Spinal ventral root avulsion results in massive motoneuron degeneration with poor prognosis and high costs. In this study, we compared different isoforms of basic fibroblast growth factor 2 (FGF2), overexpressed in stably transfected Human embryonic stem cells (hESCs), following motor root avulsion and repair with a heterologous fibrin biopolymer (HFB).
Methods: In the present work, hESCs bioengineered to overexpress 18, 23, and 31 kD isoforms of FGF2, were used in combination with reimplantation of the avulsed roots using HFB.
J Neuropathol Exp Neurol
February 2024
Graduate School of Science and Engineering, Soka University, Tokyo, Japan.
In the axotomized facial nucleus (axotFN), the levels of choline acetyltransferase, vesicular acetylcholine transporter, and gamma amino butyric acid A receptor α1 are decreased, after which the microglia begin to proliferate around injured motoneuron cell bodies. We conjectured that an injury signal released from the injured motoneurons triggers the microglial proliferation in the axotFN. However, it is unclear whether the level of microglial proliferation is dependent on the degree of motoneuronal insult.
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