Research on role of Nampt in regulating ERK1/2 in pathological myocardial hypertrophy / 中国药理学通报

Aim To investigate the role of Nampt in regulating ERK1/2 in cardiac hypertrophy and its mechanisms. Methods The primary neonatal rat cardiomyocytes were stimulated by phenylephrine (PE) (100 μmol · L

Effect of ERK1/2 Phosphorylation on Proliferation of Human Aortic Vascular Smooth Muscle Cells stimulated by Advanced Glycation End Products / 实用医学杂志

Objective To investigate the effect of ERK1/2 phosphorylation on the proliferation of human aorta vascular smooth muscle cells (HAVSMCs) stimulated by advanced glycation end products (AGEs) Methods CCK8 was used to test the effect of AGEs with different concentration on the proliferation of HAVSMCs, and the effect of PD98059, a specific inhibitor of ERK1/2, on HAVSMCs proliferation stimulated by AGEs was also detected. Flow Cytometer (FCM) was used to detect the cell cycle transformation induced by AGEs. Western Blot was used to detect the expression of relative proteins. Results 10 mg/L AGEs observably facilitated the proliferation and the DNA synthesis of HAVSMCs and PD98059 (40 umol/L) markedly inhibited the proliferation and cell cycle evolution of HAVSMCs induced by AGEs. Furthermore, ERK1/2 phosphorylation, and PCNA were regulated by AGEs and thus it showed time and dose dependent. Conclusion AGEs participates in the proliferation of HAVSMCs by activating ERK1/2 signal path.

Phosphorylation and Expression of Extracellular Signal-regulated Kinase in Cerebral Ischemic Preconditioning Rats / 中国康复理论与实践

@#Objective To explore initially the role of extracellular signal-regulated kinase (ERK1/2) in cerebral ischemic preconditioning. Methods Healthy adult SD rats were randomly divided into 5 groups: normal control group; sham group; ischemic preconditioning or ischemia tolerance group; bee venom group; peripheral noxious tolerance group. SDS-PAGE, Western blot and Gel Doc imagine systems were applied to determine the ERK1/2 phosphorylation and protein expression in somatosensory cortex and hippocampus of rats. Results The phosphorylation level of ERK1 in somatosensory cortex increased significantly (P<0.05) after ischemic preconditioning, while no significant changes in ERK2 and that of ERK1/2 in hippocampus. No significant changes in ERK1/2 protein expression were found both in somatosensory cortex and hippocampus after ischemic preconditioning. Conclusion The increased ERK1 phosphorylation level in somatosensory cortex may be involved in cerebral ischemic preconditioning.