Anti-inflammatory and neuroprotective effects of triptolide on traumatic brain injury in rats

Traumatic brain injury (TBI) is characterized by neuroinflammation, brain edema, and cerebral damage leading to impairment of neurobehavioral function. Triptolide (PG-490), a diterpenoid component from Tripterygium wilfordii Hook F., has anti-inflammatory properties. Whether triptolide has neuroprotective functions when treating TBI is unclear. To investigate this possibility, Sprague-Dawley rats were treated with triptolide immediately after TBI had been induced by a controlled cortical impact procedure or after a sham procedure. TBI produced neuroinflammation when measured on day 1 after TBI, induced cerebral damage when measured on day 1 and day 3, and impaired neurobehavioral functioning over a 28-day observation period. Triptolide suppressed TBI-induced increases in contusion volume, cell apoptosis, edema and the levels of various pro-inflammatory mediators in the brain. Thriptolide reversed the TBI-induced decrease in brain levels of anti-inflammatory cytokine interleukin-10. Importantly, triptolide improved neurobehavioral outcomes regarding motor, sensory, reflex and balance function. We conclude that triptolide confers neuroprotection against TBI, at least in part, via its anti-inflammatory activity.

► We investigated neuroprotective functions of triptolide in treating traumatic brain injury (TBI) in a rat model. ► Triptolide suppressed TBI-induced increases in contusion volume, cell apoptosis, edema and the levels of various pro-inflammatory mediators in the brain. ► Thriptolide reversed the TBI-induced decrease in brain levels of anti-inflammatory cytokine. ► Triptolide improved neurobehavioral outcomes. ► Triptolide confers neuroprotection against TBI, at least in part, via its anti-inflammatory activity.