Low Dose of Apelin-36 Attenuates ER Stress-Associated Apoptosis in Rats with Ischemic Stroke.
Low Dose of Apelin-36 Attenuates ER Stress-Associated Apoptosis in Rats with Ischemic Stroke.
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低剂量的 Apelin-36 可减弱缺血性中风大鼠内质网应激相关的细胞凋亡。
DOI：
10.3389/fneur.2017.00556
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发表时间：
2017
影响因子：
3.4
通讯作者：
Bai B
中科院分区：
文献类型：
--
作者：
Qiu J;Wang X;Wu F;Wan L;Cheng B;Wu Y;Bai B
脑缺血/再灌注（I/R）损伤诱导的细胞凋亡导致缺血性脑卒中的神经元死亡，而内质网应激（ERS）以及随后引发的未折叠蛋白反应（UPR）是脑I/R损伤诱导凋亡的主要机制。大量研究表明，apelin - 13可保护神经元免受I/R损伤诱导的凋亡。apelin - 36是apelin最长的异构体，与apelin受体的亲和力比apelin - 13更强。然而，apelin - 36在缺血性脑卒中中的作用研究较少。此外，大多数研究采用预防性给予apelin的方式，这无法准确反映其在缺血性脑卒中中的治疗潜力。在此，我们首次报道，在缺血性脑卒中发生后给予低剂量的apelin - 36（而非apelin - 13）可显著减少大鼠的梗死体积。此外，apelin - 36减轻了脑I/R损伤诱导的凋亡和半胱天冬酶 - 3的激活。进一步地，apelin - 36抑制了I/R损伤诱导的CHOP和GRP78升高，表明apelin - 36抑制了ERS/UPR的激活。我们的研究首次证明，脑卒中后给予低剂量的apelin - 36可减轻脑I/R损伤诱导的梗死和凋亡，这与抑制脑I/R损伤诱导的ERS/UPR激活有关。我们的数据支持apelin - 36在缺血性脑卒中中的治疗潜力，尽管还需要进一步的研究。
Cerebral ischemia/reperfusion (I/R) injury-induced cellular apoptosis contributes to neuronal death in ischemic stroke, while endoplasmic reticulum stress (ERS) and subsequently triggered unfolded protein response (UPR) are the major mechanisms of cerebral I/R injury-induced apoptosis. A number of studies indicated that apelin-13 protects neurons from I/R injury-induced apoptosis. Apelin-36, the longest isoform of apelin, has stronger affinity to apelin receptor than apelin-13 does. However, the role of apelin-36 in ischemic stroke is less studied. In addition, preventive administration of apelin was applied in most studies, which could not precisely reflect its therapeutic potential in ischemic stroke. Here, we first reported that low dose of apelin-36, other than apelin-13, administrated after ischemic stroke significantly reduced infarct volume in rats. Moreover, apelin-36 attenuated cerebral I/R injury-induced apoptosis and caspase-3 activation. Furthermore, apelin-36 suppressed I/R injury-induced CHOP and GRP78 elevation, indicating that apelin-36 inhibited ERS/UPR activation. Our study first demonstrated that post-stroke administration of low-dose apelin-36 could attenuate cerebral I/R injury-induced infarct and apoptosis, which is associated with the inhibition of cerebral I/R injury-induced ERS/UPR activation. Our data support the therapeutic potential of apelin-36 in ischemic stroke although further investigation is needed.
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