کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2068762 | 1078348 | 2013 | 9 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Oxygen glucose deprivation causes mitochondrial dysfunction in cultivated rat hippocampal slices: Protective effects of CsA, its immunosuppressive congener [D-Ser]8CsA, the novel non-immunosuppressive cyclosporin derivative Cs9, and the NMDA receptor anta Oxygen glucose deprivation causes mitochondrial dysfunction in cultivated rat hippocampal slices: Protective effects of CsA, its immunosuppressive congener [D-Ser]8CsA, the novel non-immunosuppressive cyclosporin derivative Cs9, and the NMDA receptor anta](/preview/png/2068762.png)
We have introduced a sensitive method for studying oxygen/glucose deprivation (OGD)-induced mitochondrial alterations in homogenates of organotypic hippocampal slice cultures (slices) by high-resolution respirometry. Using this approach, we tested the neuroprotective potential of the novel non-immunosuppressive cyclosporin (CsA) derivative Cs9 in comparison with CsA, the immunosuppressive CsA analog [D-Ser]8CsA, and MK 801, a N-methyl-d-aspartate (NMDA) receptor antagonist. OGD/reperfusion reduced the glutamate/malate dependent (and protein-related) state 3 respiration to 30% of its value under control conditions. All of the above drugs reversed this effect, with an increase to > 88% of the value for control slices not exposed to OGD. We conclude that Cs9, [D-Ser]8CsA, and MK 801, despite their different modes of action, protect mitochondria from OGD-induced damage.
Journal: Mitochondrion - Volume 13, Issue 5, September 2013, Pages 539–547