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首页> 外文期刊>International journal of peptide research and therapeutics >Apelin-13 Inhibits Apoptosis of Cortical Neurons Following Brain Ischemic Reperfusion Injury in a Transient Model of Focal Cerebral Ischemia
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Apelin-13 Inhibits Apoptosis of Cortical Neurons Following Brain Ischemic Reperfusion Injury in a Transient Model of Focal Cerebral Ischemia

机译：Apelin-13抑制局灶性脑缺血短暂性脑缺血再灌注损伤后皮质神经元的凋亡。

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摘要

Stroke is the third leading cause of death worldwide, affecting 15 million people annually. Diminished blood supply to the brain cells is the main cause of damage following stroke. When focal ischemia occurs, the core of brain tissue influenced by reduced blood supply undergoes necrotic cell death. The adipocytokine Apelin is a peptide that was isolated from a bovine stomach for the first time. This peptide and its receptor are abundantly expressed in the nervous and cardiovascular systems. According to previous studies, Apelin-13 protects cardiomyocytes from ischemic injury and apoptosis. In addition, this peptide has neuroprotective effect on hippocampal and cultured mouse cortical neurons against NMDA receptor-mediated excito-toxicity as well as cortical neurons from ischemic injury. The present study was conducted to determine whether Apelin-13 inhibits apoptosis in the ischemic penumbra in transient focal cerebral ischemia. Focal cerebral ischemia was induced in male Wistar rats by 60 min middle cerebral artery occlusion (MCAO) using a filament method,followed by 23-h reperfusion. Saline as a vehicle and Apelin-13 at doses of 50 and 100 lg were injected intra-cerebro-ventriculary (ICV) at the beginning of ischemia. Apoptosis and neurological dysfunction were assessed 24-h after MCAO. Our results indicated that administration of Apelin-13 at doses of 50 and 100 lg ICV markedly reduced apoptosis by decreasing positive TUNEL cells (P 0.001). In addition, Apelin-13 at doses of 100 lg significantly change neurological dysfunction (P 0.05). Our findings demonstrate that treatment by Apelin-13 exerts its protective effects in ischemic models via blocking programmed cell-death. We suggest that Apelin-13 might be a promising therapeutic target for stroke, although more researches are necessary to take into account the potential therapeutic effects of Apelin-13 in stroke patients.
机译：中风是全球第三大死亡原因，每年影响1500万人。脑卒中后，导致脑细胞供血减少的主要原因。当发生局灶性缺血时，受血液供应减少影响的脑组织核心会发生坏死性细胞死亡。脂肪细胞因子Apelin是一种首次从牛胃中分离的肽。该肽及其受体在神经和心血管系统中大量表达。根据以前的研究，Apelin-13保护心肌细胞免受缺血性损伤和细胞凋亡。另外，该肽对海马和培养的小鼠皮层神经元以及NMDA受体介导的兴奋性毒性以及缺血性损伤的皮层神经元具有神经保护作用。本研究旨在确定Apelin-13是否在短暂性局灶性脑缺血中抑制缺血半影中的凋亡。雄性Wistar大鼠在60分钟的大脑中动脉闭塞（MCAO）后采用细丝法诱导局灶性脑缺血，然后再进行23小时再灌注。在缺血开始时，将盐作为载体和50和100 lg的Apelin-13分别注射到脑室内。 MCAO后24小时评估细胞凋亡和神经功能障碍。我们的结果表明，以50和100 lg ICV的剂量施用Apelin-13可通过减少阳性TUNEL细胞显着减少凋亡（P 0.001）。此外，剂量为100 lg的Apelin-13可显着改变神经功能障碍（P 0.05）。我们的发现表明，Apelin-13的治疗可通过阻断程序性细胞死亡在缺血模型中发挥其保护作用。我们建议Apelin-13可能是中风的有希望的治疗靶标，尽管有必要进行更多的研究来考虑Apelin-13对中风患者的潜在治疗作用。

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