Description | Apelin-13 triTFA is the endogenous ligand of the APJ receptor, activating this G protein-coupled receptor with an EC50 value of 0.37 nM. |
In vivo | Apelin-13显著提高了AQP4表达,并降低了神经评分和梗死体积。Apelin-13在两种类型的小鼠中都通过减少BBB的渗透性、增加血管内皮生长因子、上调内皮型一氧化氮合酶和下调可诱导型NOS来发挥保护BBB的作用。在形态学上,我们通过电子显微镜检测证明了Apelin-13抑制了紧密连接的开放和内皮细胞的膨胀。同时,Apelin-13还减轻了星形胶质细胞的凋亡和促进了血管生成[1]。Apelin 13治疗显著减少了梗死大小,改善了神经功能结果,减少了脑水肿,并抑制了细胞凋亡、氧化应激和神经炎症后的I/R。Apelin 13显著增加了Nrf2的表达和AMPK及GSK-3β的磷酸化水平[2]。 |
Animal experiments | The expression of AQP4 induced by Apelin-13 injection at 1, 3, and 7 days after middle cerebral artery occlusion.?Meanwhile, examined the effects of Apelin-13 on neurological function, infarct volume, and BBB disruption owing to cerebral ischemia in wild type mice, and tested whether such effects were AQP4 dependent by using AQP4 knock-out mice[1]. |
molecular weight | 1892.89 |
Molecular formula | C75H114F9N23O22S |
Storage | keep away from moisture | Powder: -20°C for 3 years | In solvent: -80°C for 1 year |
Solubility | DMSO: 30 mg/mL (15.85 mM) |
References | 1. Chu H , Yang X , Huang C , et al. Apelin-13 Protects against Ischemic Blood-Brain Barrier Damage through the Effects of Aquaporin-4[J]. Cerebrovascular Diseases, 2017:10-25. 2. Duan J , Cui J , Yang Z , et al. Neuroprotective effect of Apelin 13 on ischemic stroke by activating AMPK/GSK-3β/Nrf2 signaling[J]. Journal of Neuroinflammation, 2019, 16(1). |