The role of diphenhydramine HCl on tumor necrosis factor-α levels in wistar rats with traumatic brain injury: An in vivo study

Abstract

Background: Traumatic brain injury (TBI) is a major cause of death and disability worldwide that imposes a significant burden on both individuals and their families. Many of the symptoms experienced by patients with TBI are thought to be mediated by the neuroinflammatory process that occurs after the primary injury. Therefore, the present study aimed to determine the effect of diphenhydramine HCl (DPM) on serum levels of the inflammatory cytokine tumor necrosis factor-α (TNF-α) after TBI. Materials and methods: This was an experimental study with a pre- and post-test control group design. A total of 10 adult Wistar rats were divided into 2 groups, the DPM group and the placebo group. The effect of DPM on serum levels of TNF-α was evaluated at 30 min, 2 h, and 24 h after the induction of experimental TBI in the rats using Marmarou's weight-drop model. Results: TNF-α levels in the DPM group significantly decreased from 0 min to 24 h after TBI (p = 0.004). In the placebo group, TNF-α levels significantly increased from 0 min to 24 h after TBI (p < 0.001). Post hoc analysis found that TNF-α levels in the DPM group decreased significantly from 30 min to 2 h and from 2 h to 24 h after TBI (p = 0.019 and p = 0.005, respectively). Conclusion: The results of this study suggest that administration of DPM causes a reduction in serum levels of TNF-α, indicating that DPM has a significant anti-inflammatory effect in experimental rats after TBI. HIGHLIGHTS Primary and secondary injuries affect traumatic brain injury's (TBI) pathogenesis. Tumor necrosis factor-α (TNF-α) is an important mediator of tissue injury. TBI increases TNF-α levels in rat models. Diphenhydramine HCl (DPM) significantly reduces TNF-α levels in rats with TBI. DPM has a significant anti-inflammatory effect in experimental rats with TBI.

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