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Effects of sinapic Acid of 4 vessel occlusion model-induced ischemia and cognitive impairments in the rat.

Kim YO, Lee SW, Oh MS, Lee HJ - Clin Psychopharmacol Neurosci (2011)

Bottom Line: To examine the neuroprotective effects of SA, SA was administrated for 14 d before 4-vessel occlusion.In this study, the efficacy of SA for the prevention of neuronal damage and for the reduction of memory impairment was investigated.The results indicate that SA confers significant neuroprotection especially for ischemic hippocampal neurons.

View Article: PubMed Central - PubMed

Affiliation: Department of Herbal Crop Research, National Institute of Horticultural & Herbal Science, Rural Development Administration, Eumseong, Korea.

ABSTRACT

Objective: Sinapic acid (SA, Sinapine), small naturally occurring hydroxycinnamic acid, has a GABA(A) receptor agonistic property and free radical scavenging activity. We examined potential neuroprotective effects of sinapic acid (SA) using global cerebral ischemia animal model.

Methods: MTT assay was performed to determine cytotoxic effects of SA. To examine the neuroprotective effects of SA, SA was administrated for 14 d before 4-vessel occlusion. Also, to determine whether SA prevents cognitive impairment, Morris water maze was performed.

Results: In this study, the efficacy of SA for the prevention of neuronal damage and for the reduction of memory impairment was investigated.

Conclusion: The results indicate that SA confers significant neuroprotection especially for ischemic hippocampal neurons.

No MeSH data available.


Related in: MedlinePlus

Neuroprotective effects of SA (1, 3, and 10 mg/kg). Either saline of SA was injected in i.p. into the animals following 10 min ischemia. Seven days later, neuronal cell density in CA1 neurons. Statistically significant differences from saline-treated group (†p<0.005, ‡p<0.001). Control, Normal animals (n=8); 4-VO, saline-treated animals following ischemia (n=8). SA, SA treated animals following ischemia (n=8 for 1, 3, and 10 mg/kg, respectively). The male wistar rats were 6 weeks.
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Figure 2: Neuroprotective effects of SA (1, 3, and 10 mg/kg). Either saline of SA was injected in i.p. into the animals following 10 min ischemia. Seven days later, neuronal cell density in CA1 neurons. Statistically significant differences from saline-treated group (†p<0.005, ‡p<0.001). Control, Normal animals (n=8); 4-VO, saline-treated animals following ischemia (n=8). SA, SA treated animals following ischemia (n=8 for 1, 3, and 10 mg/kg, respectively). The male wistar rats were 6 weeks.

Mentions: To examine the neuroprotective effect of SA, a dose of 10 mg/kg was injected i.p. into rats 0 and 90 min after the induction of cerebral ischemia. For the ischemia group, 0.89% physiological saline was injected at a volume of 180µl. When reperfusion is conducted after cerebral ischemia caused by 4-VO, pyramidal neurons in the hippocampus CA1 subfield are the most susceptible to the ischemia and start undergoing cell death 72 h after reperfusion. In the present study, rats were sacrificed 7 days after reperfusion, the time point by which all signs of neuronal cell damage have become manifest. There was no significant difference in body temperature between ischemic and SA treated groups at any time point recorded indicating that neuroprotective effects of SA were not due to a decrease in body temperature. Normal CA1 pyramidal neurons from three hemispherical sections each having a size of 1×1 mm2, were counted and averaged. In the ischemic group the viable cell density was 20.6±3.9 cells/mm2, which is far lower than that in the sham group, 303.7±4.8 cells/mm2. In the group injected with SA, viable cells were measured to be 26.9±3.1, 49.4±9.2, and 226.4±22.6 cells/mm2 at 1, 3, and 10 mg/kg. Thus SA rescued 72.7% of the ischemic neurons at 10 mg/kg injected (Fig. 2).


Effects of sinapic Acid of 4 vessel occlusion model-induced ischemia and cognitive impairments in the rat.

Kim YO, Lee SW, Oh MS, Lee HJ - Clin Psychopharmacol Neurosci (2011)

Neuroprotective effects of SA (1, 3, and 10 mg/kg). Either saline of SA was injected in i.p. into the animals following 10 min ischemia. Seven days later, neuronal cell density in CA1 neurons. Statistically significant differences from saline-treated group (†p<0.005, ‡p<0.001). Control, Normal animals (n=8); 4-VO, saline-treated animals following ischemia (n=8). SA, SA treated animals following ischemia (n=8 for 1, 3, and 10 mg/kg, respectively). The male wistar rats were 6 weeks.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3569082&req=5

Figure 2: Neuroprotective effects of SA (1, 3, and 10 mg/kg). Either saline of SA was injected in i.p. into the animals following 10 min ischemia. Seven days later, neuronal cell density in CA1 neurons. Statistically significant differences from saline-treated group (†p<0.005, ‡p<0.001). Control, Normal animals (n=8); 4-VO, saline-treated animals following ischemia (n=8). SA, SA treated animals following ischemia (n=8 for 1, 3, and 10 mg/kg, respectively). The male wistar rats were 6 weeks.
Mentions: To examine the neuroprotective effect of SA, a dose of 10 mg/kg was injected i.p. into rats 0 and 90 min after the induction of cerebral ischemia. For the ischemia group, 0.89% physiological saline was injected at a volume of 180µl. When reperfusion is conducted after cerebral ischemia caused by 4-VO, pyramidal neurons in the hippocampus CA1 subfield are the most susceptible to the ischemia and start undergoing cell death 72 h after reperfusion. In the present study, rats were sacrificed 7 days after reperfusion, the time point by which all signs of neuronal cell damage have become manifest. There was no significant difference in body temperature between ischemic and SA treated groups at any time point recorded indicating that neuroprotective effects of SA were not due to a decrease in body temperature. Normal CA1 pyramidal neurons from three hemispherical sections each having a size of 1×1 mm2, were counted and averaged. In the ischemic group the viable cell density was 20.6±3.9 cells/mm2, which is far lower than that in the sham group, 303.7±4.8 cells/mm2. In the group injected with SA, viable cells were measured to be 26.9±3.1, 49.4±9.2, and 226.4±22.6 cells/mm2 at 1, 3, and 10 mg/kg. Thus SA rescued 72.7% of the ischemic neurons at 10 mg/kg injected (Fig. 2).

Bottom Line: To examine the neuroprotective effects of SA, SA was administrated for 14 d before 4-vessel occlusion.In this study, the efficacy of SA for the prevention of neuronal damage and for the reduction of memory impairment was investigated.The results indicate that SA confers significant neuroprotection especially for ischemic hippocampal neurons.

View Article: PubMed Central - PubMed

Affiliation: Department of Herbal Crop Research, National Institute of Horticultural & Herbal Science, Rural Development Administration, Eumseong, Korea.

ABSTRACT

Objective: Sinapic acid (SA, Sinapine), small naturally occurring hydroxycinnamic acid, has a GABA(A) receptor agonistic property and free radical scavenging activity. We examined potential neuroprotective effects of sinapic acid (SA) using global cerebral ischemia animal model.

Methods: MTT assay was performed to determine cytotoxic effects of SA. To examine the neuroprotective effects of SA, SA was administrated for 14 d before 4-vessel occlusion. Also, to determine whether SA prevents cognitive impairment, Morris water maze was performed.

Results: In this study, the efficacy of SA for the prevention of neuronal damage and for the reduction of memory impairment was investigated.

Conclusion: The results indicate that SA confers significant neuroprotection especially for ischemic hippocampal neurons.

No MeSH data available.


Related in: MedlinePlus