Ischemic cerebrovascular disease is one of the most common causes of death in the World. Exogenous activin A (ActA) protects neurons against toxicity and plays a central role in regulating the brain’s response to injury. In the present study, we investigated the mechanisms involved in the neuroprotective effects of ActA in a model of hypoxic-ischemic brain disease. We found that ActA could effectively increase the survival rate of PC12 cells and relieve oxygen-glucose deprivation (OGD) damage. To clarify the neuroprotective mechanisms of ActA, the effects of ActA on the ActA/Smad pathway and on the up-regulation of inducible nitric oxide synthase (NOS) and superoxide dismutase (SOD) were investigated using OGD in PC12 cells. The results showed that ActA could increase the expression of activin receptor IIA (ActRIIA), Smad3 and Smad4 and that 50 ng/mL and 100 ng/mL of ActA could reduce NO levels and increase SOD activity by 78.9% and 79.9%, respectively. These results suggested that the neuroprotective effects of ActA in ischemia could be related to the activation of the ActA/Smad signaling pathway and to its anti-oxidant activities.
Background. Oxidative stress due to reactive oxygen species plays a central role in pathophysiology of neurodegenerative diseases. Inhibition of mitogen-activated protein kinase (MAPK) cascades attenuates the oxidative induced cell stress and behaves as potential neuroprotection agent. Materials and Methods. In this study, we evaluate hydrogen peroxide induced neural cell stress and determine how different MAPK inhibitors restore the cell damage. Results. The results indicated that oxidative stress induced by neural cell damage commonly exists, and MAPK inhibitors partially and selectively attenuated the cell damage by reducing ROS production and cell apoptosis. The cultured neurons are more susceptible to hydrogen peroxide than subculture cells. Conclusion. We conclude that the essential role of different MAPK inhibitors is to attenuate the hydrogen peroxide induced neuronal cell damage. Those data broaden the implication between individual neural cells and different MAPK inhibitors and give clues for oxidative stress induced neural diseases.
Long non-coding RNA GATA6 antisense RNA 1 (lncRNA GATA6-AS) is a recently identified lncRNA that is involved in endothelial-mesenchymal transition. The present study aimed to investigate the involvement of GATA6-AS in the progression of mantle cell lymphoma (MCL). It was found that plasma lncRNA GATA6-AS expression level was downregulated in patients with MCL, compared with that in healthy controls. Downregulation of lncRNA GATA6-AS has potential diagnostic value in early stage MCL. Overexpression of lncRNA GATA6-AS resulted in inhibited glucose uptake in the human cell lines JVM-2 and Z-138 MCL. Inhibited expression of glucose transporter 1 (GLUT1) was observed in MCL cells following lncRNA GATA6-AS overexpression, whilst GLUT1 overexpression did not alter the expression of lncRNA GATA6-AS. Additionally, lncRNA GATA6-AS overexpression inhibited, whilst GLUT1 overexpression promoted the proliferation of JVM-2 and Z-138 MCL cells; GLUT1 overexpression partially reversed the inhibitory effects of lncRNA GATA6-AS overexpression. It was therefore concluded that lncRNA GATA6-AS may inhibit cancer cell proliferation in MCL by downregulating GLUT1.
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