Institute of Physiology, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
Respir Physiol Neurobiol. 2012 Jun 15;182(1):1-8. doi: 10.1016/j.resp.2012.01.016. Epub 2012 Feb 17.
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.
创伤性脑损伤（TBI）的特征是神经炎症、脑水肿和脑损伤，导致神经行为功能障碍。雷公藤红素（PG-490）是从雷公藤中提取的二萜类成分，具有抗炎作用。雷公藤红素在治疗 TBI 时是否具有神经保护作用尚不清楚。为了研究这种可能性，Sprague-Dawley 大鼠在 TBI 诱导后立即接受雷公藤红素治疗，TBI 通过皮质撞击程序诱导或假手术诱导。TBI 在 TBI 后第 1 天测量时引起神经炎症，在第 1 天和第 3 天测量时引起脑损伤，并在 28 天观察期内损害神经行为功能。雷公藤红素抑制 TBI 诱导的挫伤体积增加、细胞凋亡、水肿和脑中各种促炎介质的水平。雷公藤红素逆转了 TBI 诱导的抗炎细胞因子白细胞介素-10 脑水平下降。重要的是，雷公藤红素改善了运动、感觉、反射和平衡功能等神经行为结局。我们得出结论，雷公藤红素通过其抗炎活性对 TBI 具有神经保护作用。
