Abstract
Traumatic brain injury (TBI) is one of the leading causes of mortality worldwide and leads to persistent cognitive, sensory, motor dysfunction, and emotional disorders. TBI-caused primary injury results in structural damage to brain tissues. Following the primary injury, secondary injuries which are accompanied by neuroinflammation, microglial activation, and additional cell death subsequently occur. Platonin, a cyanine photosensitizing dye, has been used to treat trauma, ulcers, and some types of acute inflammation. In the present study, the neuroprotective effects of platonin against TBI were explored in a controlled cortical impact (CCI) injury model in mice. Treatment with platonin (200 µg/kg) significantly reduced the neurological severity score, general locomotor activity, and anxiety-related behavior, and improved the rotarod performance of CCI-injured mice. In addition, platonin reduced lesion volumes, the expression of cleaved caspase-3, and microglial activation in TBI-insulted brains. Platonin also suppressed messenger (m)RNA levels of caspase-3, caspase-1, cyclooxygenase-2, tumor necrosis factor-α, interleukin-6, and interleukin-1β. On the other hand, free radical production after TBI was obviously attenuated in platonin-treated mice. Treatment with platonin exhibited prominent neuroprotective properties against TBI in a CCI mouse model through its anti-inflammatory, anti-apoptotic, and anti-free radical capabilities. This evidence collectively indicates that platonin may be a potential therapeutic medicine for use with TBIs.
Highlights
Traumatic brain injury (TBI) is defined as damage to the brain resulting from an external mechanical force, such as that caused by rapid acceleration or deceleration, blast waves, crushing, impacts, or penetration by a projectile [1]
Experimental and clinical studies have provided additional evidence that neuroinflammation in TBIs involves the upregulation of reactive oxygen species (ROS), cyclooxygenase (COX) enzyme, prostaglandin E2 (PGE2), and caspase-1, which contribute to cellular damage and subsequent apoptosis [15,16,17]
Platonin Improves Neurobehavioral Functions in Mice Subjected to TBI
Summary
Traumatic brain injury (TBI) is defined as damage to the brain resulting from an external mechanical force, such as that caused by rapid acceleration or deceleration, blast waves, crushing, impacts, or penetration by a projectile [1]. Experimental and clinical studies have provided additional evidence that neuroinflammation in TBIs involves the upregulation of ROS, cyclooxygenase (COX) enzyme, prostaglandin E2 (PGE2), and caspase-1, which contribute to cellular damage and subsequent apoptosis [15,16,17]. The neuroprotective ability of platonin in ischemic brain injury may be attributed to its anti-inflammatory, antithrombotic, and free radical-scavenging effects [24]. On the basis of the anti-inflammatory and neuroprotective properties of platonin, which are intimately related to brain injuries, we hypothesized that platonin might be a potential therapeutic agent against TBIs. in consideration of the critical role of the formation of excessive free radicals in the pathology of TBI, the in vivo scavenging activity of platonin against ROS was determined in the present study
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