Update on the role of cannabinoid receptors after ischemic stroke.

Update on the role of cannabinoid receptors after ischemic stroke.
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DOI:
10.1155/2012/824093
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发表时间:
2012
影响因子:
4.6
通讯作者:
Montecucco F
Montecucco F
中科院分区:
医学3区
文献类型:
--
作者:
Capettini LS;Savergnini SQ;da Silva RF;Stergiopulos N;Santos RA;Mach F;Montecucco F

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大麻素被认为是炎症性疾病(包括动脉粥样硬化)病理生理学中的关键介质。特别是,它们已被证明可以减少急性心血管事件(如急性心肌梗死和缺血性中风)后的缺血性损伤。这些对外周组织和循环炎症的保护和抗炎特性已被证明涉及它们与选择性大麻素1型(CB 1)和2型(CB 2)跨膜受体的结合。另一方面,最近发现的新型不同类别的大麻素和受体增加了动脉粥样硬化中该系统的复杂性。虽然只有初步的数据已经报道了新的大麻素受体的活动,一些研究已经调查了CB1和CB2受体在缺血性中风中的作用。虽然CB1受体激活已被证明可直接减少动脉粥样硬化斑块炎症,但有关卒中后神经传递和神经保护的数据存在争议。鉴于其对循环白细胞的有效抗炎活性,CB2活化已被证明对急性卒中后炎症产生保护作用。在本文中,我们将更新关于不同大麻素触发途径的证据,以减少急性缺血性卒中中的炎症和神经元损伤。
Cannabinoids are considered as key mediators in the pathophysiology of inflammatory diseases, including atherosclerosis. In particular, they have been shown to reduce the ischemic injury after acute cardiovascular events, such as acute myocardial infarction and ischemic stroke. These protective and anti-inflammatory properties on peripheral tissues and circulating inflammatory have been demonstrated to involve their binding with both selective cannabinoid type 1 (CB1) and type 2 (CB2) transmembrane receptors. On the other hands, the recent discoveries of novel different classes of cannabinoids and receptors have increased the complexity of this system in atherosclerosis. Although only preliminary data have been reported on the activities of novel cannabinoid receptors, several studies have already investigated the role of CB1 and CB2 receptors in ischemic stroke. While CB1 receptor activation has been shown to directly reduce atherosclerotic plaque inflammation, controversial data have been shown on neurotransmission and neuroprotection after stroke. Given its potent anti-inflammatory activities on circulating leukocytes, the CB2 activation has been proven to produce protective effects against acute poststroke inflammation. In this paper, we will update evidence on different cannabinoid-triggered avenues to reduce inflammation and neuronal injury in acute ischemic stroke.