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. 2012:2012:168756.
doi: 10.1155/2012/168756. Epub 2012 Mar 13.

Neuroprotective effect of phosphocreatine on focal cerebral ischemia-reperfusion injury

Tiegang Li  1 , Nana Wang, Min Zhao
Affiliations

Neuroprotective effect of phosphocreatine on focal cerebral ischemia-reperfusion injury

Tiegang Li et al. J Biomed Biotechnol. 2012.

Abstract

Phosphocreatine (PCr) is a natural compound, which can donate high-energy phosphate group to ADP to synthesize ATP, even in the absence of oxygen and glucose. At present, it is widely used in cardiac and renal ischemia-reperfusion (IR) disease. In this study, to examine the protective efficacy of PCr against cerebral IR, disodium creatine phosphate was injected intravenously into rats before focal cerebral IR. Intracranial pressure (ICP), neurological score, cerebral infarction volume, and apoptotic neurons were observed. Expression of caspase-3 and aquaporin-4 (AQP4) was analyzed. Compared with IR group, rats pretreated with PCr had better neurologic score, less infarction volume, fewer ultrastructural histopathologic changes, reduced apoptosis, and lower aquaporin-4 level. In conclusion, PCr is neuroprotective after transient focal cerebral IR injury. Such a protection might be associated with apoptosis regulating proteins.

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Figures

Figure 1
Figure 1
Intracranial pressure of five groups. There were no obviously differences of ICP among five groups in serial time points.
Figure 2
Figure 2
Apoptosis index in brain slices of five groups at 24 h and 72 h. Data are presented as means ± SD. *P < 0.01, versus sham-operated group. There were significant differences of apoptosis index in IR, P1, P2, P3 groups than that in sham-operated group; †P < 0.05, versus IR group. There were significant differences of apoptosis index in P1, P2, P3 groups than that in IR group; ‡versus P1 group. There were significant apoptosis in P2 and P3 groups. But, in 72 h, there was no obvious difference between P2 and P3 group.
Figure 3
Figure 3
Caspase-3 positive cells in brain slices of five groups at 24 h and 72 h. Data are presented as means ± SD. *P < 0.01, versus sham-operated group. There were significant differences in IR, P1, P2, P3 groups than that in sham-operated group; †P < 0.05, versus IR group. There were significant differences in P1, P2, P3 groups than that in IR group; ‡versus P1 group. There were significant apoptosis in P2, P3 groups. But, in 72 h, there was no obvious difference between P2 and P3 group.
Figure 4
Figure 4
(a) Apoptosis cells in brains by TUNEL assay after 24 h ischemia (×400). (b) Apoptosis cells in brains by TUNEL assay at 72 h ischemia (×400). (c) Apoptosis cells in brains by caspase-3 immunohistochemical stain assay after 24 h ischemia (×400). (d) Apoptosis cells in brains by caspase-3 immunohistochemical stain assay after 72 h ischemia (×400).
Figure 5
Figure 5
(a) Hippocampus ultrastructural histopathologic changes in five groups at 24 h (×5000). (b) Hippocampus ultrastructural histopathologic changes in five groups at 72 h (×5000).
Figure 6
Figure 6
Western Blot analyses of AQP4. 32 and 34 kDa representing the two AQP4 protein isoforms expressed in brain.
Figure 7
Figure 7
AQP4 relative density of five groups. *P < 0.01, versus sham-operated group; †P < 0.05, versus IR group. There were significant differences in P1, P2, P3 groups than that in IR group. But there was no obvious differences between P1, P2, and P3 groups in AQP4 relative density.
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