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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

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.
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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.

Mentions: In the ischemia group, increased caspase-3 immunoreactivity was found in the cortex and subcortex regions. Caspase-3 immunoreactivity was widely observed along the ischemic zone. Within the ischemic area, some cells exhibited necrotic cell morphology and vacuolization. In the ischemia group, there was an increase in immunopositive cells around the damaged brain tissue. Caspase-3 immunoreactivity in the ischemia + SA6 and ischemia + SA24 groups was significantly less than that in the ischemia group and was similar to that in the control group (Figures 5, 6). Caspase-3 immunoreactivity in the ischemia + SA6 and ischemia + SA24 groups was significantly less than in the ischemia group (P < 0.05). In the ischemia + SA6 group, caspase-9 immunoreactivity was similar to that in the ischemia + SA24 group. Around the large cortical neurons, caspase-9 immunoreactive cells were ring-shaped while they were granular within the nucleus. Immunoreactivity for caspase-9 was intense in the pyramidal cells in the ischemia group, and caspase-9 immunopositivity was also present in the endothelial cells of the veins (Figures 5, 6).


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)

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.
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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.
Mentions: In the ischemia group, increased caspase-3 immunoreactivity was found in the cortex and subcortex regions. Caspase-3 immunoreactivity was widely observed along the ischemic zone. Within the ischemic area, some cells exhibited necrotic cell morphology and vacuolization. In the ischemia group, there was an increase in immunopositive cells around the damaged brain tissue. Caspase-3 immunoreactivity in the ischemia + SA6 and ischemia + SA24 groups was significantly less than that in the ischemia group and was similar to that in the control group (Figures 5, 6). Caspase-3 immunoreactivity in the ischemia + SA6 and ischemia + SA24 groups was significantly less than in the ischemia group (P < 0.05). In the ischemia + SA6 group, caspase-9 immunoreactivity was similar to that in the ischemia + SA24 group. Around the large cortical neurons, caspase-9 immunoreactive cells were ring-shaped while they were granular within the nucleus. Immunoreactivity for caspase-9 was intense in the pyramidal cells in the ischemia group, and caspase-9 immunopositivity was also present in the endothelial cells of the veins (Figures 5, 6).

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