TARGETING NEUROINFLAMMATION IN TRAUMATIC BRAIN INJURY: A PHARMACOLOGICAL APPROACH
Madhu Vashisht, Anurag Bhargava, Minky Mukhija, Mohit Kumar* and Anjali
ABSTRACT
Traumatic brain injury (TBI) is linked to higher mortality and long-term abnormalities in neurocognition, making it a major worldwide health concern. Following traumatic brain injury (TBI), neuroinflammation is a crucial target for pharmaceutical management due to its role in secondary injury mechanisms such as neuronal death, axonal damage, and disruption of the blood-brain barrier. The possibility of reducing the negative effects of traumatic brain injury by modifying the neuroinflammatory response is examined in this review. Pro-inflammatory cytokines and small-molecule medications also reduce inflammation by activating the glucocorticoid receptor, but anti-inflammatory cytokines function to control inflammation. Microglial activation and cytokine release are inhibited by the antibiotic minocycline, which also has anti-inflammatory qualities. Cyclooxygenase inhibitors are among the non-steroidal anti-inflammatory medications (NSAIDs) that reduce inflammation by preventing the formation of prostaglandins. Statins, which are mainly used for hyperlipidaemia, have demonstrated the ability to modulate inflammation through the inhibition of leukocyte migration and the reduction of inflammatory biomarkers. Clinical trials have yielded inconsistent results, despite promising preclinical results, underscoring the need for more investigation. This review emphasizes the need for a multimodal therapy approach and the complexity of neuroinflammation in traumatic brain injury. Personalized medicine, cutting-edge drug delivery methods, and synergistic therapy could be the next big things in treatment efficacy, which could lead to better rehabilitation outcomes for patients with traumatic brain injuries.
Keywords: Anti-Inflammatory Cytokines, Corticosteroids, Minocycline, Neuroinflammation, Pharmacological Interventions, Traumatic Brain Injury.
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