Abstract

Background: Traumatic spinal cord injury (tSCI) is a severe neurological condition that causes long-term nerve function impairment and can even cause death. Further efforts are needed to find better therapy for this condition to improve patients' quality and life expectancy. Moleac 901 (MLC901) is a phytopharmacological refinement that incorporates important molecules to facilitate progenitor nerve cell amplification and differentiation and has significant neuroprotective effects in tSCI cases. This systematic review aims to discover the potential of MLC901 as adjuvant therapy for traumatic spinal cord injury by multi-pathway biomechanism. Methods: Researchers searched for data sources using three databases (PubMed, Science Direct, and Google Scholar) using the keywords “MLC901” and “Spinal Cord Injury.” Articles are included if related to the potential and biomechanism of MLC901 and/or its constituent components in tSCI therapy, using RCT designs, observational, animal studies, and/or original research, including national and international articles from 2013-2023. Article selection followed PRISMA's guidelines for measuring the quality of systematic reviews. Results: Total of 123 articles were obtained from the database search, and then 13 articles were identified that met the review requirements. Of the 13 articles reviewed, two were related to MLC901 therapy in tSCI: one animal study article and one cohort study in humans. In contrast, the other 11 articles are animal and pharmacological analysis studies discussing the benefits of MLC901 components for tSCI therapy. The MLC901's active ingredients, such as paeoniflorin, safflower yellow, salvianolic acid B, and astragali radix-angelicae sinensis radix, have demonstrated their potential in targeting multiple pathways involved to prevent inflammation, improve microcirculation, protect damaged nerve cells, and promote nerve repair and regeneration. Conclusion: MLC901 acts primarily as an adjuvant treatment for spinal cord injury by promoting a neuroprotective effect, inhibiting apoptosis, stimulating neurite growth, and reducing pro-inflammatory cytokines.

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