Table 1.
Summary of postconditioning studies in cerebral ischemia
| Reference | S | Model |
Postconditioning |
Infarct reduction | Mechanisms and behavioral test | ||||
|---|---|---|---|---|---|---|---|---|---|
| Onset | Ocl | Rep | Cycle | ||||||
| (Zhao et al, 2006) | R | pMCAo, CCAo, 15 min | 30 secs | 10 secs | 30 secs | 3 | 80% | Inhibits generation of free radical and apoptosis (TUNEL staining) | |
| 30 min | 30 secs | 10 secs | 30 secs | 3 | 51% | ||||
| 60 min | 30 secs | 10 secs | 30 secs | 3 | 17% | ||||
| (Pignataro et al, 2008) | R | Focal, 100 min | 2 min | 2 min | 2 min | 5 | 23% (not significant) | Akt, but not ERK and p38 activity, contributes to the protection of postconditioning. All the above pathways contribute to the protection of preconditioning. Combination of postconditioning with preconditioning offers no synergistic effect | |
| 5 min | 5 min | 5 min | 3 | 38% | |||||
| 10 min | 10 min | N/A | 1 | 65% | |||||
| 30 min | 10 min | N/A | 1 | NP | |||||
| 120 min OGD, cell culture | 60 min | 30 min | N/A | 1 | NP | ||||
| 30 min | 10 min | N/A | 1 | NP | |||||
| 10 min | 30 min | N/A | 1 | NP | |||||
| 10 min | 10 min | N/A | 1 | ∼24% | |||||
| (Xing et al, 2008b) | R | MCAo, 60 min | 30 secs | 30 secs | 30 secs | 6 | ∼14% at 1 day | Inhibits cytochrome c release, caspase-3 activity and DNA fragmentation; enhances SOD and Bcl-2 expression; improves neurological scores | |
| ∼12% at 3 days | |||||||||
| (Gao et al, 2008a) | R | pMCAo, 30 min CCAo | 30 secs | 30 secs | 10 secs | 3 | 33% at 2 days | Improved CBF at 30 min after CCA release. Combination of preconditioning with postconditioning offered no additional protection | |
| 30 secs | 30 secs | 10 secs | 10 | NP | |||||
| 10 secs | 10 secs | 10 secs | 3 | NP | |||||
| 10 secs | 10 secs | 10 secs | 10 | 56% | |||||
| 3 min | 10 secs | 10 secs | 10 | NP | |||||
| (Gao et al, 2008b) | R | pMCAo, 30 min CCAo | 30 secs | 30 secs | 10 secs | 3 | 39% at 1 month after stroke | Akt pathway contributes to the protection of postconditioning; both MAPK and PKC pathways are involved in the protective mechanisms | |
| (Wang et al, 2008) | R | Global 4 VO, 10 min | 15 secs | 15 secs | 15 secs | 3 | Hipp | ∼70%, 7days | Improves CBF; attenuates cytochrome c release; improves spatial learning and memory |
| ∼77%, 14 days | |||||||||
| Cortex | ∼98%, 7 days | ||||||||
| ∼98%, 14 days | |||||||||
| 30 secs | 30 secs | 30 secs | 3 | Hipp | ∼51%, 7 days | ||||
| ∼67%, 14 days | |||||||||
| Cortex | ∼76%, 7 days | ||||||||
| ∼83%, 14 days | |||||||||
| 60 secs | 15 secs | 60 secs | 3 | Hipp | NP, 7 days | ||||
| NP, 14 days | |||||||||
| Cortex | NP, 7 days | ||||||||
| NP, 14 days | |||||||||
| 45 secs | 15 secs | 15 secs | 3 | Hipp | ∼94%, 7 days | ||||
| ∼94%, 14 days | |||||||||
| Cortex | ∼96%, 7 days | ||||||||
| ∼93%, 14 days | |||||||||
| (Rehni and Singh, 2007) | M | Global, 2 VO, 10 min | 10 secs | 10 secs | 10 secs | 3 | No morphological study | Akt inhibition contributes to postconditioning. Postconditioning improves behavioral tests | |
| (Burda et al, 2006a) | R | 4 VO 8 min | 2 days | 5 min | N/A | 1 | ∼94%, 7days | Cycloheximide, inhibitor of protein synthesis, blocks postconditioning's protection | |
| NE | N/A | 1 | ∼100%, 7days | ||||||
| 10 min | 2 days | 6 min | N/A | 1 | ∼100%, 7days | ||||
| 15 min | 3-NP | N/A | 1 | ∼75%, 7days | |||||
| (Danielisova et al, 2006) | R | 10 min | 2 days | 5 min | N/A | 1 | ∼90%, 7 days | Increased SOD activity | |
| (Danielisova et al, 2008) | R | 8 min | 2 days | Bradykinin | N/A | 1 | ∼91%, 3days, by Fluoro Jade B staining | Postconditioning inhibits changes in MnSOD and CuZnSOD activity | |
| (Scartabelli et al, 2008) | R | 30 min OGD, slice culture | 5 min | 3 min, OGD | N/A | 1 | ∼33% | mGlu1 and mGlu5 antagonists and PI3K–Akt inhibitor abolish protection of postconditioning Combination of preconditionong and postconditioning has no additive protection | |
| 3 min, DHPG | N/A | 1 | ∼56% | ||||||
| 15 min | N/A | 1 | ∼44% | ||||||
| 30 min | N/A | 1 | NP | ||||||
| (Lee et al, 2008) | R | 15 min OGD, Slice culture | Immediately or 10 min later | 1%, 1.5%, 2%, 2.5%, 3% isoflu, for 10, 30, 60 or 80 min | N/A | 1 | 2% isoflu for 30 min applied immediately after OGD reduced ∼36%; 2% isoflu for 30 min applied 10 min also protected | KATP channel blockers inhibit the protection of postconditioning | |
| 90 min MCAo | Immediately | 60 min 2% isoflu | N/A | 1 | ∼48% | ||||
| (Ren et al, 2008) | R | pMCAo, 30 min CCAo* | 10 secs | 10 secs | 10 secs | 10 | ∼50% | Delayed postconditioning improves metabolism, attenuates BBB leakage and edema formation, and inhibits t-PA exacerbated-brain injury. It mitigates behavioral deficits up to 2 months after stroke | |
| 3 h | 10 secs | 10 secs | 10 | NP | |||||
| 30 secs | 30 secs | 30 secs | 3 | ∼39% | |||||
| 3 h | 30 secs | 30 secs | 3 | ∼44% | |||||
| # | 3 h | 15 min | 15 min | 6 | ∼46% | ||||
| 6 h | 15 min | 15 min | 6 | ∼64% | |||||
The typical protocol for performing postconditioning is shown in Figure 1. The onset time, occlusion (Ocl), and reperfusion (Rep) time are documented. The percentage of infarct size reduced by postconditioning is also summarized; when the exact number of infarct size was not reported in the cited literatures, infarct reduction was approximately estimated from the bar graphs. The potential protective mechanisms and the outcomes of behavioral tests are also summarized. S, species; R. rat; M, mouse; PMCAo, CCAo, permanent middle cerebral artery occlusion combined with bilateral common carotid artery occlusion; Focal, focal ischemia; Global, global ischemia; OGD, oxygen glucose deprivation; 2 or 4 VO, 2 or 4 vessel occlusion; Ocl, occlusion; Rep, reperfusion; N/A, non applicable; NP, no protection.
Postconditioning was induced by bilateral CCA occlusion and release.
postconditioning was performed by the ipsilateral CCA occlusion and release.