Evaluation of Neuroprotective and Neuroregenerative Potential of NeuroAiD™ II(MLC901) in a Rat Model of Kainic Acid-Induced Spinal Cord Injury

Abstract

Excitotoxic damage caused by high extracellular levels of glutamate in the spinal cord results in neuronal loss and severe locomotor impairment. This study investigates the efficacy of NeuroAiD II (MLC901), an herbal formulation, in promoting nerve regeneration following spinal cord injury (SCI) induced by kainic acid (KA). KA, a potent glutamate receptor agonist, causes excitotoxic damage in the spinal cord, leading to neuronal loss and locomotor impairment. To explore the potential of MLC901, KA-injured rats were treated with MLC901, and nerve regeneration was evaluated using various techniques. In this study, KA was administered intrathecally between the T12 and T13 vertebrae in rats, resulting in incomplete paraplegia. MLC901 was then tested for its neuro-regenerative potential. Various assessments were conducted to evaluate the effects of MLC901 treatment, including behavioral, electrophysiological, and histopathological analyses. Behavioral tests, such as the Basso, Beattie, and Bresnahan (BBB) open field test, running wheel, grid walk, inverted grid, and sensory tests, showed significant improvements in locomotor activity in treated rats. Electrophysiological recordings indicated that, while KA injection caused reduced amplitude and delayed latency, MLC901 treatment helped restore lost connections on days 14 and 28. Histopathological and immunohistochemical analyses also revealed improved tissue integrity and neuron survival. The study concludes that MLC901 significantly enhances locomotor recovery, somatosensory evoked potentials, and tissue preservation following SCI. These findings suggest that MLC901 holds promise as a neuro-regenerative therapy for spinal cord injuries.

Keywords: GAP43; GFAP; Glutamate receptors agonist; Kainic acid excitotoxicity; Nerve regeneration; NeuroAiD II (MLC 901); Spinal cord injury.