Open AccessThis article is
- freely available
Molecular Dissection of Cyclosporin A’s Neuroprotective Effect Reveals Potential Therapeutics for Ischemic Brain Injury
Aquatic Animal Health Division, National Research Institute of Aquaculture, Fisheries Research Agency, Tamaki, Mie 519-0423, Japan
Received: 23 June 2013; in revised form: 30 July 2013 / Accepted: 14 August 2013 / Published: 5 September 2013
Abstract: After the onset of brain ischemia, a series of events leads ultimately to the death of neurons. Many molecules can be pharmacologically targeted to protect neurons during these events, which include glutamate release, glutamate receptor activation, excitotoxicity, Ca2+ influx into cells, mitochondrial dysfunction, activation of intracellular enzymes, free radical production, nitric oxide production, and inflammation. There have been a number of attempts to develop neuroprotectants for brain ischemia, but many of these attempts have failed. It was reported that cyclosporin A (CsA) dramatically ameliorates neuronal cell damage during ischemia. Some researchers consider ischemic cell death as a unique process that is distinct from both apoptosis and necrosis, and suggested that mitochondrial dysfunction and Δψ collapse are key steps for ischemic cell death. It was also suggested that CsA has a unique neuroprotective effect that is related to mitochondrial dysfunction. Here, I will exhibit examples of neuroprotectants that are now being developed or in clinical trials, and will discuss previous researches about the mechanism underlying the unique CsA action. I will then introduce the results of our cDNA subtraction experiment with or without CsA administration in the rat brain, along with our hypothesis about the mechanism underlying CsA’s effect on transcriptional regulation.
Keywords: ischemic cell death; neuroprotective agent; cyclosporin-A; transcriptional regulation
Article StatisticsClick here to load and display the download statistics.
Notes: Multiple requests from the same IP address are counted as one view.
Cite This Article
MDPI and ACS Style
Kawakami, M. Molecular Dissection of Cyclosporin A’s Neuroprotective Effect Reveals Potential Therapeutics for Ischemic Brain Injury. Brain Sci. 2013, 3, 1325-1356.
Kawakami M. Molecular Dissection of Cyclosporin A’s Neuroprotective Effect Reveals Potential Therapeutics for Ischemic Brain Injury. Brain Sciences. 2013; 3(3):1325-1356.
Kawakami, Minoru. 2013. "Molecular Dissection of Cyclosporin A’s Neuroprotective Effect Reveals Potential Therapeutics for Ischemic Brain Injury." Brain Sci. 3, no. 3: 1325-1356.