Anjum Anam, Yazid Muhammad Dain, Daud Muhammad Fauzi, Idris Jalilah, Ng Angela Min Hwei, Naicker Amaramalar Selvi, Ismail Ohnmar Htwe Rashidah, Athi Kumar Ramesh Kumar, Lokanathan Yogeswaran
Department of Tissue Engineering and Regenerative Medicine, Faculty of Medicine, Universiti Kebangsaan Malaysia, 56000, Kuala Lumpur, Cheras, Malaysia.
University of Maryland School of Medicine, Baltimore, MD, 21201, USA.
Mol Neurobiol. 2025 Jun 6. doi: 10.1007/s12035-025-05064-4.
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.
脊髓中细胞外谷氨酸水平过高导致的兴奋性毒性损伤会导致神经元丧失和严重的运动功能障碍。本研究调查了草药配方NeuroAiD II（MLC901）在促进由海藻酸（KA）诱导的脊髓损伤（SCI）后神经再生方面的疗效。KA是一种强效谷氨酸受体激动剂，会在脊髓中造成兴奋性毒性损伤，导致神经元丧失和运动功能障碍。为了探索MLC901的潜力，对KA损伤的大鼠进行MLC901治疗，并使用各种技术评估神经再生情况。在本研究中，将KA经鞘内注射到大鼠的T12和T13椎骨之间，导致不完全性截瘫。然后测试MLC901的神经再生潜力。进行了各种评估以评估MLC901治疗的效果，包括行为学、电生理学和组织病理学分析。行为测试，如Basso、Beattie和Bresnahan（BBB）旷场试验、跑步轮试验、网格行走试验、倒置网格试验和感觉测试，显示治疗大鼠的运动活动有显著改善。电生理记录表明，虽然注射KA导致振幅降低和潜伏期延迟，但MLC901治疗有助于在第14天和第28天恢复失去的连接。组织病理学和免疫组织化学分析也显示组织完整性和神经元存活率有所改善。该研究得出结论，MLC901可显著增强SCI后的运动恢复、体感诱发电位和组织保存。这些发现表明，MLC901有望成为一种用于脊髓损伤的神经再生疗法。
