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INNOSC Theranostics and
Pharmacological Sciences Antioxidant effects of curcumin in SCI
that CuC treatment can decrease the levels of MDA, We also investigated the protein concentrations of
induce the activation of GSH peroxidase, and ameliorate inflammatory mediators, specifically ASC, NLRP3,
OS in rat models. Dong et al. investigated the effects of and Casp-1, at the injury site. Our findings revealed a
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CuC in a mouse wound model by administering it into significant increase in these markers after SCI. The results
the abdominal cavity. Their findings indicated that CuC also showed a dramatic reduction in the concentrations of
exhibited a protective effect on nerve tissue. This effect NLRP3, ASC, and Casp1 proteins in the animals receiving
was related to the upregulation of nuclear factor erythroid 40 and 80 mg/kg of CuC, in comparison to the Model
2-related factor 2 (Nrf2), a key regulator of the antioxidant group animals. This suggests a noteworthy decrease in the
response. The study also noted the upregulation of levels of these inflammatory proteins. Prior studies have
downstream antioxidant enzymes, suggesting that CuC demonstrated that CuC can substantially enhance recovery
may enhance the body’s ability to combat OS and promote following SCI by fostering the development of new nerve
nerve protection and recovery following injury. In 2018, cells (neurogenesis) and modulating inflammatory
Caillaud et al. conducted research to explore the impact pathways. For example, research conducted by Lee et al.
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of continuous topical treatment with low doses of CuC on revealed that administering CuC orally at a dosage of
nerve function and regeneration after sciatic nerve injury 0.4 mg/kg for 2 weeks led to an increase in neurogenesis by
in mice. These findings indicate that CuC has a protective affecting brain-derived neurotrophic factor concentrations
effect against OS by reducing the secretion of ROS generated in the hippocampus, a crucial area of the brain involved
by macrophages. In addition, it lowers lipid peroxidation in learning and memory. The results of another study
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levels and boosts the expression of the transcription factor revealed that administering a low dose of CuC (exceeding
Nrf2, which plays a crucial role in regulating antioxidant 0.2 mg/kg) resulted in an increase in the generation of
responses. Furthermore, applying low doses of CuC locally new cells within the hippocampus, thereby enhancing
shows potential as an effective treatment for peripheral neurogenesis in adult mice. Barati et al. investigated the
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nerve regeneration. These findings are consistent with the CuC effects on rats with SCI. They found that CuC might
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results of our current research. help improve movement in the early stages of the injury
In addition to the assessment of OS parameters, by promoting nerve repair and reducing the inflammation
functional recovery was evaluated in the present research. caused by astrocyte activity. The results of the mentioned
The BBB test outcomes showed a notable reduction in studies were in accordance with the results of this study
scores of BBB for animals with SCI in comparison to the related to the inflammasome complex.
Control group animals. Among the animals treated with Numerous studies have consistently shown that CuC
40 and 80 mg/kg CuC, we observed a meaningful elevation effectively mitigates OS. This protective effect is achieved
in the BBB scores relative to the untreated SCI animals. through multiple mechanisms including: (1) reducing lipid
Kim et al. assessed the effects of CuC on the development peroxidation products such as MDA, 4-hydroxynonenal,
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of SCI in a rat model. They found that CuC (200 mg/kg) and protein carbonyls, (2) enhancing the activity of GSH
significantly improved functional recovery in the early peroxidase and SOD, which are essential antioxidant
stages following SCI. Furthermore, they presented that enzymes, and (3) activating the Nrf2, a crucial regulator of
CuC decreased the MDA levels, increased the activity of the body’s antioxidant response. 39-41 Despite the potential
SOD, and reduced the inflammation. The results of this health benefits CuC can offer, taking large amounts can
study are in agreement with the findings of Kim et al.’s lead to unpleasant side effects such as stomach upset,
research. The findings of the mentioned studies are in nausea, dizziness, gastroesophageal reflux disease, and
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line with the outcomes of the present study. Research diarrhea, and our findings proved that consuming CuC at
conducted by Alvarado-Sanchez et al. demonstrated moderate dose could mitigate SCI development.
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that CuC effectively reduced concentrations of hydroxyl
radicals, nitric oxide, and lipid peroxidation following SCI, 5. Conclusion
although it did not significantly affect SOD activity. Our
results align with these findings; however, we observed This study found that moderate and high doses of CuC
significant effects of CuC on SOD activity, which contrast effectively reduced OS and inflammation caused by SCI.
with the outcomes reported by Alvarado-Sanchez et al. Since a marked decrease was not noted between animals
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This discrepancy may be attributed to the timing of the OS receiving varying CuC doses, a moderate dose of CuC is
parameter measurements. In our study, we assessed the recommended.
levels of OS parameters 4 weeks post-SCI and treatment, Acknowledgments
whereas their study evaluated these parameters just 24 h
after SCI. None.
Volume 8 Issue 2 (2025) 83 doi: 10.36922/itps.4795

