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非诺贝特,一种过氧化物酶体增殖物激活受体α激动剂,在创伤性脑损伤中发挥神经保护作用。

Fenofibrate, a peroxisome proliferator-activated receptor alpha agonist, exerts neuroprotective effects in traumatic brain injury.

作者信息

Besson Valérie C, Chen Xiao R, Plotkine Michel, Marchand-Verrecchia Catherine

机构信息

Université Paris Descartes, Faculté de Pharmacie, Laboratoire de Pharmacologie de la Circulation Cérébrale, UPRES EA 2510, 4 avenue de l'Observatoire, F-75006 Paris, France.

出版信息

Neurosci Lett. 2005 Nov 4;388(1):7-12. doi: 10.1016/j.neulet.2005.06.019.

Abstract

Peroxisome proliferator-activated receptor alpha (PPARalpha) has been demonstrated to reduce inflammation in various inflammatory diseases. As traumatic brain injury (TBI) caused a neuroinflammatory response, we examined the effect of fenofibrate, a PPARalpha agonist, on the post-traumatic consequences caused by lateral fluid percussion of brain in rats. The effects of fenofibrate (50 and 100mg/kg) were evaluated on the consequences of TBI in the early phase (6 and 24h) and the late phase (7 days) after TBI. Neurological deficit, brain lesion, cerebral oedema and ICAM-1 expression were evaluated. Treatment with fenofibrate (given p.o. at 1 and 6h after TBI) decreases the neurological deficit induced by TBI at 24h. Furthermore, fenofibrate reduces brain oedema and ICAM-1 expression at 24h post-TBI. Rats given fenofibrate at 1, 6, 24, 48 and 72h after TBI show neurological recovery associated with a reduction of the brain lesion at 7 days post-TBI. The present data represents the first demonstration that fenofibrate, a PPARalpha agonist, exerts neuroprotective effects in TBI. The activation of receptor PPARalpha could be beneficial by counteracting the deleterious inflammatory response following TBI. This suggests that PPARalpha activation could be a new and promising therapeutic strategy for the treatment of brain trauma.

摘要

过氧化物酶体增殖物激活受体α(PPARα)已被证明可减轻多种炎症性疾病中的炎症反应。由于创伤性脑损伤(TBI)会引发神经炎症反应,我们研究了PPARα激动剂非诺贝特对大鼠脑侧流体冲击所致创伤后后果的影响。评估了非诺贝特(50和100mg/kg)对TBI早期(6和24小时)和晚期(7天)后TBI后果的影响。评估了神经功能缺损、脑损伤、脑水肿和ICAM-1表达。非诺贝特治疗(在TBI后1和6小时口服给药)可降低TBI在24小时时诱导的神经功能缺损。此外,非诺贝特可减轻TBI后24小时的脑水肿和ICAM-1表达。在TBI后1、6、24、48和72小时给予非诺贝特的大鼠在TBI后7天显示出神经功能恢复,同时脑损伤减轻。目前的数据首次证明,PPARα激动剂非诺贝特在TBI中发挥神经保护作用。激活受体PPARα可能通过对抗TBI后的有害炎症反应而有益。这表明PPARα激活可能是一种治疗脑外伤的新的有前景的治疗策略。

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