The effects of melatonin in the treatment of acute brachial plexus compression injury in rats

Abstract

Introduction: Brachial plexus injury (BPI) is one of the most destructive peripheral nerve injuries and there is still a lack of effective treatment.

Methods: This study was conducted to evaluate the effects of melatonin in the treatment of acute brachial plexus compression injury in rats using histopathological, histomorphometric, immunohistochemical and electrophysiological methods. Forty-eight adult male Sprague Dawley rats were randomly allocated into three groups: sham, melatonin and vehicle groups. The brachial plexus compression injury model was performed by a vascular clamp. Melatonin group received intraperitoneal injection of melatonin at doses of 10 mg/kg for 21 days after crush injury. The conduction velocity and amplitude of compound muscle action potential (CAMP) in the regenerated nerve, and nerve histomorphometry, as well as levels of myelin protein zero (P0) protein of the crush region were assessed.

Results: Compared with the vehicle group, the melatonin group which reported significant increased CMAP conduction velocity and amplitude also showed thicker myelin sheath and lower levels of P0 protein.

Discussion: Our results suggest that melatonin effectively promotes nerve regeneration and improves the function of damaged nerves. Melatonin treatment is a promising strategy for the treatment of acute brachial plexus compression injury.

Keywords: acute brachial plexus compression injury; melatonin; myelin protein zero; nerve regeneration; rat model.

Figure 1

The modeling diagram.

Figure 2

The general views of histological sections stained by Fast blue, silver and H&E. (A–C) Sham group: well-arranged and distributed nerve fibers were observed; (D–I) vehicle groups at 7 and 14 days: typical features of peripheral nerve injury after 7 days could be seen in (D–F), including myelin loss with Wallerian degeneration (arrow), and endoneurial edema (*). (G–I) A further decrease in nerve fiber density, disruption of fiber arrangement, and a marked increase in fibrosis (triangle) and axonal vacuolization (arrowhead) at day 14. (J–O) Melatonin groups at 7 and 14 days: compared with vehicle group, less axonal degeneration and vacuolization, as well as fibrosis were observed, with more regenerating axon clusters (star) and the nerve fibers were are neatly aligned.

Figure 3

Transmission electron micrographs showing the ultrastructure of brachial plexus day 7 after injury. (A) Vehicle group; (B) melatonin group. Nerves in the melatonin group showed thicker myelin sheaths and narrower endoneural gaps compared to the vehicle group. Scale bar = 5 mm.

Figure 4

P0 protein/GAPDH protein levels were assessed using western blotting in the injured sites of rats in all 3 groups, 3 weeks after injury. p-value ^* < 0.05.