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The peripheral nervous system (PNS) connects muscles, organs, and glands to the central nervous system (CNS) via nerves. Traumatic accidents can cause partial or total loss of motor and sensory functions, with limited regenerative potential affected by factors like age, injury type, and timing of intervention. Molecular therapy, including Inosine (IN), has shown promise in promoting axon regeneration, have immunomodulatory and neuroprotective properties, being a therapeutic potential in pathological processes.
This study aims to characterize IN's mechanisms in the PNS and proteins involved in early stages using proteomic analysis on mice with sciatic crush model. Sixty female C57BL6, aged between 8-10 weeks mice were divided into three groups: IN-treated injured, saline-treated injured, and uninjured. After 4 days, nerves were extracted, quantified for electrophoresis, protein hydrolysis and the samples were analysed by a mass spectrometer and using bioinformatics tools.
Comparing with saline group, IN-treated mice showed higher protein expression related to cellular processes like morphogenesis and organism development, suggesting axon regeneration promotion. IN group exhibited more proteins involved in cellular components like cytosol and synapse, particularly in axonal guidance and protein metabolism, indicating enhanced axonal communication in the regenerative process. Moreover, treated animals displayed increased proteins related to synaptic and cell junction processes, along with immune system pathways, possibly indicating an early response to injury and potential inflammation control.
These findings shed light on IN's role in repairing peripheral nervous tissue, offering insights into new molecular targets for traumatic PNS injury treatment.
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