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. 2014 Nov 1;9(21):1884-90.
doi: 10.4103/1673-5374.145353.

Syringaldehyde exerts neuroprotective effect on cerebral ischemia injury in rats through anti-oxidative and anti-apoptotic properties

Affiliations

Syringaldehyde exerts neuroprotective effect on cerebral ischemia injury in rats through anti-oxidative and anti-apoptotic properties

Aras Adem Bozkurt et al. Neural Regen Res. .

Abstract

There are few studies on the neuroprotective effects of syringaldehyde in a rat model of cerebral ischemia. The study aimed to elucidate the mechanisms underlying the neuroprotective effects of syringaldehyde on ischemic brain cells. Rat models of cerebral ischemia were intraperitoneally administered syringaldehyde. At 6 and 24 hours after syringaldehyde administration, cell damage in the brain of cerebral ischemia rats was obviously reduced, superoxide dismutase activity and nuclear respiratory factor 1 expression in the brain tissue were markedly increased, malondiadehyde level was obviously decreased, apoptosis-related cysteine peptidase caspase-3 and -9 immunoreactivity was obviously decreased, and neurological function was markedly improved. These findings suggest that syringaldehyde exerts neuroprotective effects on cerebral ischemia injury through anti-oxidation and anti-apoptosis.

Keywords: apoptosis; brain ischemia; inflammatory; nerve regeneration; neural regeneration; neuroprotective effects; oxidative stress; syringaldehyde.

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Conflict of interest statement

Conflicts of interest: None declared.

Figures

Figure 1
Figure 1
Superoxide dismutase (SOD, U/mg protein) activity, malonedialdehyde (MDA, nmol/mL per mg protein) and nuclear respiratory factor-1 (NRF1, nmol/mL per mg protein) levels in brain tissue of rats. The comparisons among four groups were made by one-way analysis of variance followed by the Bonferroni post test. Data were expressed as the mean ± SD. *P < 0.05, vs. ischemia and control groups. #P > 0.05, vs. ischemia + SA6 group. SA6: 6 hours after syringaldehyde adminis-tration; SA24: 24 hours after syringaldehyde administration.
Figure 2
Figure 2
Representative pathomorphological photomicrographs of ischemic rat brain tissue stained with hematoxylin-eosin. (A) Ischemia group; (B) ischemia + SA6 group; (C) ischemia + SA24 group; (D) control group. Compared to the ischemia group, red neurons were reduced in the ischemia + SA6 and ischemia + SA24 groups. Red neurons (rc), edema (e) and vacuolization (v) are shown. Scale bars: 20 μm. SA6: 6 hours after syringaldehyde administration; SA24: 24 hours after syringaldehyde administration.
Figure 3
Figure 3
Representative photomicrographs showing neurons stained with Luxol Fast Blue in the ischemic brain area of rats at 6 and 24 hours after syringaldehyde treatment. (A) Ischemia group; (B) ischemia + SA6 group; (C) ischemia + SA24 group; (D) control group. Vascular dilatation (di) and red neurons (rc) are shown. Scale bars: 20 μm. SA6: 6 hours after syringaldehyde administration; SA24: 24 hours after syringaldehyde administration.
Figure 4
Figure 4
Effect of SA on edema, red neurons, vacuolization and neuronal degeneration in ischemic brain at 6 and 24 hours after middle cerebral artery occlusion. Neuronal cells in the area were counted to determine cell density. Data were expressed as percentiles and compared between groups using the Kruskal Wallis test. Data were expressed as the mean ± SD. *P < 0.05, vs. ischemia group. #P < 0.05, vs. control group. SA6: 6 hours after syringaldehyde administration; SA24: 24 hours after syringaldehyde administration.
Figure 5
Figure 5
Caspase-3 (A1–D1) and caspase-9 (A2–D2) immunoreactivities in the ischemic brain tissue at 6 and 24 hours after syringaldehyde treatment. The representative example of immunohistochemical images in ischemia group (A1–A2), ischemia + SA6 group (B1, B2), ischemia + SA24 group (C1, C2) and control group (D1, D2). Immunoreactivity for caspase-3 and -9 in neurons (arrows) and perinuclear areas (arrowheads) are shown. Vacuolization (v) is shown. Caspase-3 and -9 immunoreactivities decreased in the ischemia + SA6 and ischemia + SA24 groups compared to the ischemia group. Scale bars: 20 μm. SA6: 6 hours after syringaldehyde administration; SA24: 24 hours after syringaldehyde administration.
Figure 6
Figure 6
Effect of syringaldehyde on caspase-3 and -9 immunoreactivities in ischemic brain tissue of rats. Data expressed as percentiles. *P < 0.05, vs. ischemia group; #P > 0.05, vs. control group. Data comparison between groups was performed using Kruskal Wallis tests. SA6: 6 hours after syringaldehyde administration; SA24: 24 hours after syringaldehyde administration.
Figure 7
Figure 7
Effect of syringaldehyde on Bederson scores in rats with cerebral ischemia injury. Data expressed as the mean ± SD. *P < 0.05, vs. ischemia group; #P < 0.05, vs. ischemia + SA6 group. The comparisons among four groups were made by one-way analysis of variance followed by the Bonferroni post test. SA6: 6 hours after syringaldehyde administration; SA24: 24 hours after syringaldehyde administration.

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