Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
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Cell. Physiol. Biochem. · Jan 2014
Repeated administration of ketamine can induce hippocampal neurodegeneration and long-term cognitive impairment via the ROS/HIF-1α pathway in developing rats.
Recent animal experiments have suggested that ketamine administration during development might induce widespread neurodegeneration and long-term cognitive deficits. The underlying mechanism is not fully understood. ⋯ We suggest that ketamine-induced neurodegeneration in neonatal rats, followed by long-term cognitive deficits, might be mediated via the ROS/HIF-1α pathway.
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Cell. Physiol. Biochem. · Jan 2014
Panax quinquefolium saponin attenuates cardiomyocyte apoptosis and opening of the mitochondrial permeability transition pore in a rat model of ischemia/reperfusion.
Opening of the mitochondrial permeability transition pore (mPTP) is a critical event during ischemia/reperfusion (I/R) injury. Recently, we showed that Panax quinquefolium saponin (PQS) alleviates apoptosis of cardiomyocytes by suppressing excessive endoplasmic reticulum stress (ERS) during I/R injury. Here, we hypothesized that this anti-apoptotic effect might be mediated through inhibition of mPTP and the mitochondrial apoptotic pathway. ⋯ Our results show that PQS can alleviate apoptosis of cardiomyocytes during I/R injury, possibly due to repressed mitochondrial apoptotic pathway associated with the opening of mPTP induced by myocardial I/R injury.
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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.