Abstract
Purpose: To investigate the effects of myricetin on peripheral nerve regeneration in sciatic nerve crush injury model.Methods: Separate groups of rats were administered myricetin at 25, 50 or 100 mg/kg body weight/day for 2 weeks. Functional recovery following sciatic nerve injury was assessed by foot position and walking track analyses, measurement of mechanical hyperalgesia, and withdrawal reflex latency (WRL).Results: Myricetin treatment resulted in significantly enhanced recovery of sensorimotor functions as evidenced by increased scores in functional analysis tests. Myricetin treatment remarkably elevated brain derived neurotrophic factor (BDNF) expression, and also enhanced activation of Akt and mTORc1, reflecting up-regulation of PI3K/Akt/mTORC1 signalling involved in nerve regeneration.Conclusion: Myricetin enhances functional recovery and nerve regeneration in rats. These findings suggest that myricetin is a potent neuroprotective agent with potential for the management of peripheral nerve injury.Keywords: Glycogen synthase kinase 3β, Mammalian target of rapamycin (mTOR), Myricetin, Nerve regeneration
Highlights
In clinical practice, peripheral nerve injuries (PNIs) are encountered frequently due to tumours, accidental trauma, acute compression, surgeries or iatrogenic injuries
Rats treated with higher dose of myricetin (100 mg/kg) presented negligible foot location movement or any irregular foot placing from day 14 post-surgery through day 21 (Figure 1)
The myricetin-treated rats presented a marked decrease in paw withdrawal reflex thresholds (WRT) to powered stimulus, relative to saline-treated crush group from 14th to 21st day post-injury (Figure 3)
Summary
Peripheral nerve injuries (PNIs) are encountered frequently due to tumours, accidental trauma, acute compression, surgeries or iatrogenic injuries. Traumatic injuries are on the increase, with estimated 500,000 new patients every year [1]. The peripheral nerve damage results in total or partial function impairment affecting the motor, sensory and autonomic functions. Peripheral nerve injury (PNI) is characterized by disruption of axons and myelin sheaths [2]. Schwann cell tubes of the basal lamina remain intact and aid in regeneration of axons and re-innervation of tissues [3,4]. The time taken for reinnervation of the target tissues is critical for improvement in sensory and motor functions, which makes accelerated regeneration vital for adequate functional recovery [5].
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