Abstract
Spinal cord injury (SCI) is one of the most devastating medical conditions; however, currently, there are no effective pharmacological interventions for SCI. Ginsenoside Rg3 (GRg3) is one of the protopanaxadiols that show anti-inflammatory, anti-oxidant, and neuroprotective effects. The present study investigated the neuroprotective effect of GRg3 following SCI in rats. SCI was induced using a static compression model at vertebral thoracic level 10 for 5 min. GRg3 was administrated orally at a dose of 10 or 30 mg/kg/day for 14 days after the SCI. GRg3 (30 mg/kg) treatment markedly improved behavioral motor functions, restored lesion size, preserved motor neurons in the spinal tissue, reduced Bax expression and number of TUNEL-positive cells, and suppressed mRNA expression of pro-inflammatory cytokines including tumor necrosis factor-α, interleukin (IL)-1β, and IL-6. GRg3 also attenuated the over-production of cyclooxygenase-2 and inducible nitric oxide synthase after SCI. Moreover, GRg3 markedly suppressed microglial activation in the spinal tissue. In conclusion, GRg3 treatment led to a remarkable recovery of motor function and a reduction in spinal tissue damage by suppressing neuronal apoptosis and inflammatory responses after SCI. These results suggest that GRg3 may be a potential therapeutic agent for the treatment of SCI.
Highlights
Spinal cord injury (SCI) is one of the most devastating medical conditions that can temporarily or permanently impair physical functions
We evaluated the improvement of motor function and spinal tissue damage and examined the and spinaleffects tissueondamage examined the effects onmediators, neuronal and apoptosis, pro-inflammatory mediators, neuronaland apoptosis, pro-inflammatory microglial activation following the treatment with
Hindlimb behavioral motor functions were significantly impaired in the SCI group
Summary
Spinal cord injury (SCI) is one of the most devastating medical conditions that can temporarily or permanently impair physical functions. SCI is characterized by an initial physical damage (primary injury) leading to one or more progressive damaging processes (secondary injury) that spread away from the injury epicenter [1]. The initial physical injury leads to tissue necrosis and a disruption of neuronal and vascular structures. The secondary injury process is predominantly responsible for the damage associated with SCI, including inflammation, oxidative stress, ischemia, necrosis, and neuronal apoptosis [2]. Despite recent advances including transplantation of neural stem cells, tissue engineering, and molecular therapy [4,5], neurological recovery following SCI remains limited, Molecules 2017, 22, 122; doi:10.3390/molecules22010122 www.mdpi.com/journal/molecules
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