ArticleFrontiers in pharmacology2025
Exploring the neuroprotective potential of naringin following spinal cord injury in rats: improving sensory and motor function through combating inflammation and oxidative stress.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Supercritical COPharmaceutics · 2026Article
- Anxiolytic and antidepressant effects of astaxanthin: behavioral and mechanistic insights in a rat model.Frontiers in pharmacology · 2026Article
- Sappanone A Promotes Motor Function Recovery in Spinal Cord Injury Mice by Inhibiting Microglial M1 Polarization via Activation of the Keap1/Nrf2 Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
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6 authors.
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Abstract
Introduction: Spinal cord injury (SCI) leads to widespread cascades of inflammatory and oxidative factors. This pathological condition damages nerves and causes neurological disorders. To address these complex conditions, it is important to identify therapeutic candidates that affect multiple dysregulated signaling mediators and targets. Some phytochemicals such as naringin (NAI) with neuroprotective, antioxidant, and anti-inflammatory effects can be seen as a possible candidate for treating neurodegenerative diseases. Purpose: Therefore, this study aims to evaluate the impact and mechanism of NAI on sensory and motor function in rats with SCI. Materials and methods: In total, 35 rats were studied in five groups, including sham, SCI, and three groups treated with intrathecal administration of NAI (5, 10, and 15 mM). After the injury, sensorimotor behavioral tests and weight changes were performed for 4 weeks. On the 28 Results and discussion: NAI treatment demonstrated significant benefits in rats with SCI, including reducing pain, improvement in motor performance, and attenuated animal weight gain. Besides, NAI decreased the lesion area of spinal tissue and enhanced neuronal survival at both ventral and dorsal horns of spinal tissue. Furthermore, serum analysis revealed that NAI increased MMP-2 activity and catalase and glutathione levels while decreasing nitrite and MMP-9 activity. Conclusion: The intrathecal administration of NAI can be proposed as a proper alternative in the treatment of sensory-motor disorders caused by SCI through neuroprotective, anti-inflammatory, and antioxidant mechanisms.
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