Apelin-13 - CAS 217082-58-1
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A crystalline solid
Apelin-13; Apelin-13 (human, bovine, mouse, rat)
1.5 g/cm3
1.Apelin-13 administration protects against ischemia/reperfusion-mediated apoptosis through FoxO1 pathway in high-fat diet-induced obesity.
Boal F1,2, Timotin A1,2, Roumegoux J1,2, Alfarano C1,2, Calise D2,3, Anesia R1,2, Parini A1,2, Valet P1,2, Tronchere H1,2, Kunduzova O1,2. Br J Pharmacol. 2016 Mar 23. doi: 10.1111/bph.13485. [Epub ahead of print]
BACKGROUND AND PURPOSE: Apelin-13, an endogenous ligand for the APJ receptor, behaves as a potent modulator of metabolic and cardiovascular disorders. Here, we examined the effects of apelin-13 on myocardial injury in a mouse model combining ischemia/reperfusion (I/R) and obesity and explored underlying mechanisms.
2.Apelin-13 induces autophagy in hepatoma HepG2 cells through ERK1/2 signaling pathway-dependent upregulation of Beclin1.
Huang Q1, Liu X1, Cao C1, Lei J1, Han D1, Chen G1, Yu J1, Chen L2, Lv D1, Li Z3. Oncol Lett. 2016 Feb;11(2):1051-1056. Epub 2015 Dec 3.
The aim of the present study was to investigate the effect of Apelin-13 on autophagy in hepatocellular carcinoma HepG2 cells and the underlying mechanism of the effect. The HepG2 cells were treated with Apelin-13 at a final concentration of 0.0001, 0.001, 0.01 and 0.1 µmol/l for 24 h. Cells were also treated with 10 µmol/l PD98059 for 24 h. The expression of the extracellular signal-regulated kinase (ERK)1/2, phosphorylated ERK1/2 (pERK1/2) and Beclin1 proteins were detected by western blot analysis. Beclin1 mRNA expression was also detected by reverse transcription-polymerase chain reaction. Autophagy was observed using fluorescence microscopy subsequent to monodansylcadaverine (MDC) staining. Following treatment with the various concentrations of Apelin-13, the expression of the ERK1/2 protein remained at a similar level, whereas the expression of pERK1/2 increased in a dose-dependent manner. Compared with the control group, the increase was significant (P<0.
3.Activation of Endogenous Cardiac Stem Cells by Apelin-13 in Infarcted Rat Heart.
Zhang NK, Cao Y, Zhu ZM, Zheng N, Wang L, Xu XH, Gao LR. Cell Transplant. 2016 Feb 26. [Epub ahead of print]
Our previous study demonstrated that the apelin-APJ pathway contributed to myocardial regeneration and functional recovery after BMSCs transplantation during the differentiation of BMSC into cardiomyogenic cells in AMI rat models. However, the underlying mechanisms by which apelin promotes cardiac repair and functional recovery are not completely clarified. In the present study, we investigated whether apelin could mobilize and activate endogenous cardiac stem cells and progenitors, thereby mediating regeneration and repair myocardium after acute myocardial infarction in rat models. 6-wk-old Sprague Dawley male rats underwent AMI and receive apelin-13 (200ng, n=10) or an equivalent volume of saline intramyocardium injection (n=10), and a sham group (n=8). Proliferation of endogenous cardiac stem cell was analyzed by immunofluorescence staining in rat infarct myocardium, and heart function was evaluated by echocardiography examination at 28 days after apelin-13 injection.
4.Apelin-13 Protects PC12 Cells from Corticosterone-Induced Apoptosis Through PI3K and ERKs Activation.
Zou Y1, Wang B2, Fu W1, Zhou S3, Nie Y4, Tian S5. Neurochem Res. 2016 Mar 9. [Epub ahead of print]
It is widely accepted that environmental stress is a risk factor for mental disorders. Glucocorticoid hormones play a vital role in the regulation of physiological response to stress. High concentrations of corticosterone can induce cellular damage in PC12 cells, which possess typical neuronal features. Apelin and its receptor APJ are widely distributed in the central nervous system including limbic structures involved in stress responses. Previous studies have suggested that apelin has a neuroprotective function. However, the effect of apelin on corticosterone-induced neuronal damage remains to be elucidated. In the present study, we explored the potential protective activity of apelin-13 in PC12 cells treated with corticosterone and its underling mechanisms. The viability of the cells, the apoptosis of the cells, the level of phosphorylation of Akt (p-Akt) and extracellular signal-regulated kinases (p-ERKs) and cleaved caspase-3 expression were detected by MTT, Hoechst staining and flow cytometer assays and Western blotting.
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CAS 217082-58-1 Apelin-13

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