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

Bozkurt AA, Mustafa G, Tarık A, Adile O, Murat SH, Mesut K, Yıldıray K, Coskun S, Murat C - Neural Regen Res (2014)

Bottom Line: The study aimed to elucidate the mechanisms underlying the neuroprotective effects of syringaldehyde on ischemic brain cells.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, Çanakkale Onsekiz Mart University, Canakkale, Turkey.

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.

No MeSH data available.


Related in: MedlinePlus

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.
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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.

Mentions: Hematoxylin-eosin staining results showed that in the ischemia + SA6 and ischemia + SA24 groups, increased amounts of neuronal damage occurred after ischemia and there was stronger chromatin signal intensity in the nuclei. Red neurons with severe acidophilic neuronal cytoplasm, pyknotic appearance and karyorrhexis-caused neuronal damage were observed. In the ischemia + SA6 group, the number of red neurons was slightly increased compared to the control group. Red neurons were significantly reduced in number in the ischemia + SA6 group than in the ischemia group. In the ischemia + SA24 group, red neuron count was broadly similar to the amount in the control group. In the ischemia + SA6 and ischemia + SA24 groups, vacuolar areas surrounding the cells, cellular degeneration and swollen areas were significantly reduced compared to the ischemia group (Figures 2, 4).


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

Bozkurt AA, Mustafa G, Tarık A, Adile O, Murat SH, Mesut K, Yıldıray K, Coskun S, Murat C - Neural Regen Res (2014)

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.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4281426&req=5

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.
Mentions: Hematoxylin-eosin staining results showed that in the ischemia + SA6 and ischemia + SA24 groups, increased amounts of neuronal damage occurred after ischemia and there was stronger chromatin signal intensity in the nuclei. Red neurons with severe acidophilic neuronal cytoplasm, pyknotic appearance and karyorrhexis-caused neuronal damage were observed. In the ischemia + SA6 group, the number of red neurons was slightly increased compared to the control group. Red neurons were significantly reduced in number in the ischemia + SA6 group than in the ischemia group. In the ischemia + SA24 group, red neuron count was broadly similar to the amount in the control group. In the ischemia + SA6 and ischemia + SA24 groups, vacuolar areas surrounding the cells, cellular degeneration and swollen areas were significantly reduced compared to the ischemia group (Figures 2, 4).

Bottom Line: The study aimed to elucidate the mechanisms underlying the neuroprotective effects of syringaldehyde on ischemic brain cells.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, Çanakkale Onsekiz Mart University, Canakkale, Turkey.

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.

No MeSH data available.


Related in: MedlinePlus