HGF protects cultured cortical neurons against hypoxia/reoxygenation induced cell injury via ERK1/2 and PI-3K/Akt pathways

Hepatocyte growth factor (HGF) has been revealed to exert multipotent activities on a variety of cells. In this study, we investigated whether HGF had a direct neuroprotection on cultured cerebral cortical neurons subjected to hypoxia/reoxygenation (H/R) and explored the intracellular signalings mediated the effects. The decrease in cell viability and increase in number of apoptotic cells resulting from H/R were significantly prevented by HGF pre-treatment. HGF stimulated both ERK1/2 and Akt activities in cortical neurons. Inhibition of ERK activation completely abolished the protective effects of HGF, and inhibition of Akt activation reduced, but did not completely eliminate the HGF mediated neuroprotection. It is suggested that the neuroprotection of HGF depend on ERK1/2 pathway, and, to a lesser extent, PI-3K/Akt pathway. In addition, we found that pre-treatment with HGF remarkably attenuated the decrease in expression of Bcl-2 and Bcl-xL induced by H/R, but failed to affect the amount of Bax. It is likely that Bcl-2 and Bcl-xL contribute to the protective effects of HGF.     

Molecular imaging of enhanced Na expression in the liver of total sleep deprived rats by TOF-SIMS

Sleep disorder is associated with metabolic disturbances, which was related to oxidative stress and subsequently sodium overload. Since liver plays important roles in metabolic regulation, present study is aimed to determine whether hepatic sodium, together with oxidative stress, would significantly alter after total sleep deprivation (TSD). Sodium ion was investigated by time-of-flight secondary ion mass spectrometry (TOF-SIMS). Parameter for oxidative stress was examined by heat shock protein-25 (HSP-25) immunohistochemistry. TOF-SIMS spectrum indicated that hepatic Na⁺/K⁺ ratio counting as 82.41 ± 9.5 was obtained in normal rats. Sodium ions were distributed in hepatocytes with several aggregations. However, following TSD, the intensity for Na⁺/K⁺ ratio was relatively increased (101.94 ± 6.9) and signals for sodium image were strongly expressed throughout hepatocytes without spatial localization. Quantitative analysis revealed that HSP-25 staining intensity is 1.78 ± 0.27 in TSD rats, which was significantly higher than that of normal ones (0.68 ± 0.15). HSP-25 augmentation suggests that hepatocytes suffer from oxidative stress following TSD. Concerning oxidative stress induced sodium overload would impair metabolic function; enhanced hepatic sodium expression after TSD may be a major cause of TSD relevant metabolic diseases.