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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Cannabinoid CB2 receptor activation reduces mouse myocardial ischemia-reperfusion injury: involvement of cytokine/chemokines and PMN
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Cannabinoid CB2 receptor activation reduces mouse myocardial ischemia-reperfusion injury: involvement of cytokine/chemokines and PMN

机译:大麻素CB2受体激活减少小鼠心肌缺血/再灌注损伤:细胞因子/趋化因子和PMN的参与

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摘要

In this study, we have assessed the activation of the cannabinoid CB2 receptor (CB2-R) in a model of mouse myocardial ischemia/reperfusion (I/R). The results show that treatment of animals with WIN55212-2, a CB1/CB2-R agonist, given 30 min before induction of I/R, significantly reduced the extent of infarct size (IS) in the area at risk, as measured 2.5 h later, with almost a 51% inhibition observed at the dose tested of 3.5 mg/kg intraperitoneally (i.p.). The protective effect of WIN55212-2 was almost abolished by the selective CB2-R antagonist AM630 (1 mg/kg i.p.) and not affected by the selective CB1-R antagonist AM251 (3 mg/kg i.p.). The CB2-R antagonist administered alone produced a slight but significant (P0.05) increase in IS compared with vehicle alone. The protection afforded by WIN55212-2 was paralleled by lower values of myeloperoxidase activity and interleukin-1?2 and of the CXC chemokine ligand 8 into the injured tissue. In conclusion, we demonstrate for the first time that exogenous and endogenous CB2-R activation reduces the leukocyte-dependent myocardial damage associated with an I/R procedure.
机译:在这项研究中,我们评估了小鼠心肌缺血/再灌注(I / R)模型中大麻素CB2受体(CB2-R)的激活。结果表明,在诱导I / R之前30分钟给予WIN55212-2(一种CB1 / CB2-R激动剂)治疗动物,可显着降低危险区域梗塞面积(IS)的程度(2.5 h)后来,在3.5 mg / kg腹膜内(ip)的剂量下观察到几乎抑制了51%。选择性CB2-R拮抗剂AM630(1 mg / kg i.p.)几乎消除了WIN55212-2的保护作用,而不受选择性CB1-R拮抗剂AM251(3 mg / kg i.p.)的影响。与单独的媒介物相比,单独施用的CB2-R拮抗剂在IS中产生了轻微但显着(P <0.05)的增加。 WIN55212-2提供的保护与较低的髓过氧化物酶活性和白介素-1β2以及CXC趋化因子配体8进入受损组织的值相当。总之,我们首次证明了外源性和内源性CB2-R激活减少了与I / R程序相关的白细胞依赖性心肌损伤。

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