ArticleRegenerative therapy2025
Gallic acid protect against spinal cord ischemia-reperfusion injury in rat via activation of Nrf2/HO-1 signaling.
Article in Regenerative therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Emerging regenerative strategies for spinal cord injury: exosome-derived mechanisms and therapeutic insights.Frontiers in neuroscience · 2025Pooled it
- Phytochemical Profiling and Biological Evaluation of Pistacia lentiscus L. grown in Chlef (Algeria): An Integrated In Vitro, In Vivo, and In Silico Study.Chemistry & biodiversity · 2026Article
- Nrf2-Activating Natural Compounds in Neurodegenerative Diseases: Targeting Oxidative Stress and Protein Aggregation.International journal of molecular sciences · 2026Review
- Bitter gourd bioactive peptide alleviates neuronal ferroptosis after spinal cord ischemia-reperfusion injury, combined with emerging cell and animal models.Frontiers in nutrition · 2026Article
- Dual ROS/pH-responsive mangiferin-loaded smart microneedles for precision therapy of wound infections.Materials today. Bio · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Object: This study explores Gallic acid's (GA) neuroprotective effects against spinal cord ischemia-reperfusion injury (SCII) and its underlying mechanisms. Methods: Spinal cord ischemia/reperfusion injury was induced in rats using the modified Zivin's method of clamping the abdominal aorta. The Basso-Beattie-Bresnahan scores, the inclined plane test, hematoxylin and eosin (HE) staining, and Nissl staining were used to measure locomotor activity and histological changes in the injured spinal cords. Proinflammatory factors (TNF-α and IL-1β) were examined using an ELISA kit. Moreover, In vitro oxidative stress model was induced by tBHP used to assess the cell survival rate, reactive oxygen species (ROS) levels, Malondialdehyde (MDA) levels. RT-qPCR and Western blot was used to detect the expression levels of mRNA and proteins. Results: In vitro, GA inhibited tBHP-induced apoptosis in PC-12 cells, reduced ROS and MDA production, and abolished the expression of pro-apoptotic factors while enhancing the Nrf2/HO-1 signaling pathway. In vivo, GA treatment improved the behavioral and structural aspects of SCII in rats, inhibiting the production of proinflammatory factors, also reduced oxidative stress, and prevented neuronal apoptosis by enhancing the Nrf2/HO-1 signaling pathway. Conclusions: GA exhibits neuroprotective effects against SCII, involving antioxidant, anti-inflammatory, and anti-apoptotic activities through Nrf2/HO-1 signaling pathway.
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