Increased levels of tumor necrosis factor-alpha in rat with traumatic brain injury after NeuroAid (MLC 901) administration

Abstract

Background: Tumor necrosis factor-alpha (TNF-α) is an inflammatory cytokine produced by macrophages in acute inflammatory processes and plays roles in cell signaling that cause necrosis and apoptosis. This study aimed to show whether there was an effect of Neuroaid (MLC 901) on TNF-α levels in rats with traumatic brain injury (TBI) measured using the Enzyme-linked immunosorbent assay in the peripheral blood. Methods: A total of 10 Sprague-Dawley rats were divided into two groups, one group was given MLC 901 ( n = 5), and the other group was not given MLC 901 (NaCl 0.9%) ( n = 5). All groups were treated with brain injury using the modified Marmarou model. The measurements of TNF-α were performed at 30 min and 6 weeks after brain injury. Results: At 30 min after brain injury, the TNF-α level in the MLC 901 group was higher (3564.8) than the 0.9% NaCl group (3453.6), but it was not statistically significant ( P = 0.830). At 6 weeks of treatment, the TNF-α level in the MLC 901 group (2576.6) was higher than the 0.9% NaCl group (1383.4) and statistically significant ( P = 0.001). This study showed that the administration of MLC 901 could increase TNF-α levels at 6 weeks after treatment. Conclusion: MLC 901 increases TNF-α levels in rats with TBI, with a significant rise observed at 6 weeks, suggesting a sustained inflammatory response.

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