Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
-
Cell. Physiol. Biochem. · Jan 2014
Ketamine inhibits proliferation of neural stem cell from neonatal rat hippocampus in vitro.
Ketamine is a widely used anesthetic in obstetric and pediatric anesthesia. In the developing brain, the widespread neuron apoptosis triggered by ketamine has been demonstrated. However, little is known about its effect on neural stem cells (NSCs) function. This study aimed to investigate the effect of ketamine on proliferation of NSCs from neonatal rat hippocampus. ⋯ Ketamine inhibited proliferation of NSCs from neonatal rat hippocampus in vitro. Suppressing Ca(2+)-PKCα-ERK1/2 signaling pathway may be involved in this inhibitory effect of ketamine on NSCs proliferation.
-
Cell. Physiol. Biochem. · Jan 2014
Role of continuous high thoracic epidural anesthesia in hippocampal apoptosis after global cerebral ischemia in rats.
Cervical sympathetic blockade has been found to reduce cerebral vascular resistance and improve focal cerebral ischemia/reperfusion injury. In this study, we tested the hypothesis that the sympathetic blockade of high thoracic epidural anesthesia (HTEA) would reduce hippocampal apoptosis after global cerebral ischemia (GCI) injury. ⋯ Our study demonstrated that continuous HTEA attenuates hippocampal apoptosis and a behavioral deficit after global cerebral ischemia, and that these protective effects are associated with the improved microcirculation, reduced oxidative stress and the less activation of PARP.
-
Cell. Physiol. Biochem. · Jan 2013
miR-224 is critical for celastrol-induced inhibition of migration and invasion of hepatocellular carcinoma cells.
The molecular mechanisms of celastrol on hepatocellular carcinoma (HCC) cells migration and invasion ability is the major problem that prompted the study. ⋯ Celastrol treatment inhibits migration and invasion of HCC cell and that the effect is partly due to NF-κB regulating miR-224 expression.
-
Cell. Physiol. Biochem. · Jan 2013
Exogenous hydrogen sulfide protects against doxorubicin-induced inflammation and cytotoxicity by inhibiting p38MAPK/NFκB pathway in H9c2 cardiac cells.
We have demonstrated that exogenous hydrogen sulfide (H2S) protects H9c2 cardiac cells against the doxorubicin (DOX)-induced injuries by inhibiting p38 mitogen-activated protein kinase (MAPK) pathway and that the p38 MAPK/nuclear factor-κB (NF-κB) pathway is involved in the DOX-induced inflammatory response and cytotoxicity. The present study attempts to test the hypothesis that exogenous H2S might protect cardiomyocytes against the DOX-induced inflammation and cytotoxicity through inhibiting p38 MAPK/NF-κB pathway. ⋯ The present study has demonstrated the new mechanistic evidence that exogenous H2S attenuates the DOX-induced inflammation and cytotoxicity by inhibiting p38 MAPK/NF-κB pathway in H9c2 cardiac cells. We also provide novel data that the interaction between NF-κB pathway and IL-1β is important in the induction of DOX-induced inflammation and cytotoxicity in H9c2 cardiac cells.
-
Cell. Physiol. Biochem. · Jan 2013
Atorvastatin improves microenvironment to enhance the beneficial effects of BMSCs therapy in a rabbit model of acute myocardial infarction.
To investigate the beneficial effects of atorvastatin added to the cell therapy with bone marrow-derived mesenchymal stromal cells (BMSCs) in a rabbit model of acute myocardial infarction (AMI). ⋯ Atorvastatin acts to improve the microenvironment both by synergistically enhancing the existing effects of BMSCs and by adding new therapeutic effects to BMSCs transplantation, and this combinational therapy is a superior cell/pharmacological therapeutic approach that merits future preclinical and clinical studies.