Abstract
Spinal cord injury (SCI) results in permanent loss of motor function below the injured site. Neuroinflammatory reaction following SCI can aggravate neural injury and functional impairment. Ginseng is well known to possess anti-inflammatory effects. The present study investigated the neuroprotective effects of Panax ginseng C.A. Mayer (P. ginseng) after SCI. A spinal contusion was made at the T11-12 spinal cord in adult male Sprague-Dawley rats (n = 47) using the NYU impactor. Motor function was assessed using the Basso-Beattie-Bresnahan (BBB) score in P. ginseng (0.1, 0.5, 1, 3, and 5 mg/kg) or vehicle (saline) treated after SCI. We also assessed the protein expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) at the lesion site by western blot and then measured the cavity area using luxol fast blue/cresyl violet staining. P. ginseng treated group in SCI showed a significant improvement in locomotor function after the injury. The protein expression of COX-2 and iNOS at the lesion site and the cavity area were decreased following SCI by P. ginseng treatment. These results suggest that P. ginseng may improve the recovery of motor function after SCI which provides neuroprotection by alleviating posttraumatic inflammatory responses.
Highlights
Novel molecules from medicinal plants and botanicals play an important role in protecting the health as they have less side effects in comparison to synthetic therapeutic compounds [1]
We examined the neuroprotective effects of P. ginseng after Spinal cord injury (SCI)
The present data show that P. ginseng decreased the protein expression of inducible nitric oxide synthase (iNOS) and COX-2 following spinal contusion, thereby leading to enhanced functional recovery SCI
Summary
Novel molecules from medicinal plants and botanicals play an important role in protecting the health as they have less side effects in comparison to synthetic therapeutic compounds [1]. Spinal cord injury (SCI) results in permanent loss of motor function below the injury site. The available treatment alternatives are limited which can contribute to significant recovery from functional loss after SCI. Primary mechanical injury and another pathological stimulation create the injury to the secondary neuron and affect the spinal cord [2, 3]. Posttraumatic inflammation, which occurs within minutes and persists for days, is known as a possible mechanism of secondary injury after SCI [4, 5]. Previous studies have shown that nitric oxide (NO) [6], cyclooxygenase-2 (COX-2) [7], and proinflammatory cytokines [8] may contribute to the pathogenesis of secondary injury process. Management of the inflammatory reaction following SCI is important to prevent the tissue damage and protection of the cells [9]
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