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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

Effects of SA on Morris water maze performance on the probe trial deficits induced by 10 min cerebral ischemia in rats (n=8). Oral administration of SA (10 mg/kg) for 14 days. Mean daily latencies of escaping from the start point onto the hidden platform. Each rat was subjected to two trials per day for 5 consecutive days. Data represent means±SD: Control, 13.83±5.49 sec; 4VO, 23.17±4.54 sec; Nimodipine, 9.83±0.79 sec; SA, 24.5±6.57, 23.5±2.93, 10.67±0.76 sec at 1, 3, 10 mg/kg (*p<0.05, †p<0.0051).
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Figure 3: Effects of SA on Morris water maze performance on the probe trial deficits induced by 10 min cerebral ischemia in rats (n=8). Oral administration of SA (10 mg/kg) for 14 days. Mean daily latencies of escaping from the start point onto the hidden platform. Each rat was subjected to two trials per day for 5 consecutive days. Data represent means±SD: Control, 13.83±5.49 sec; 4VO, 23.17±4.54 sec; Nimodipine, 9.83±0.79 sec; SA, 24.5±6.57, 23.5±2.93, 10.67±0.76 sec at 1, 3, 10 mg/kg (*p<0.05, †p<0.0051).

Mentions: The water maze reveals an impairment in spatial learning and memory which can be easily quantified. To compare spatial learning of rat, we tested them on the hidden platform and testing 1 week after induced ischemia. Seven days following ischemia induced by 4-VO. During the escape trials all rats were able to find the hidden platform. With increasing number of trials the escape latency decreased in both groups. Latency times for the 4-VO rats were consistently longer than times for either the sham-operated or SA treated animals, as was the time to reach the platform region during the probe trial on day 6. Ischemic animals receiving SA took slightly longer to swim to the platform than sham operated animals, but performed just as well in the probe trial (Fig. 3). In the probe trials, rats after ischemia take longer than sham-operated rats. Thus prolongation of latency was markedly shortened by SA at a dose of 10 mg/kg.


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)

Effects of SA on Morris water maze performance on the probe trial deficits induced by 10 min cerebral ischemia in rats (n=8). Oral administration of SA (10 mg/kg) for 14 days. Mean daily latencies of escaping from the start point onto the hidden platform. Each rat was subjected to two trials per day for 5 consecutive days. Data represent means±SD: Control, 13.83±5.49 sec; 4VO, 23.17±4.54 sec; Nimodipine, 9.83±0.79 sec; SA, 24.5±6.57, 23.5±2.93, 10.67±0.76 sec at 1, 3, 10 mg/kg (*p<0.05, †p<0.0051).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 3: Effects of SA on Morris water maze performance on the probe trial deficits induced by 10 min cerebral ischemia in rats (n=8). Oral administration of SA (10 mg/kg) for 14 days. Mean daily latencies of escaping from the start point onto the hidden platform. Each rat was subjected to two trials per day for 5 consecutive days. Data represent means±SD: Control, 13.83±5.49 sec; 4VO, 23.17±4.54 sec; Nimodipine, 9.83±0.79 sec; SA, 24.5±6.57, 23.5±2.93, 10.67±0.76 sec at 1, 3, 10 mg/kg (*p<0.05, †p<0.0051).
Mentions: The water maze reveals an impairment in spatial learning and memory which can be easily quantified. To compare spatial learning of rat, we tested them on the hidden platform and testing 1 week after induced ischemia. Seven days following ischemia induced by 4-VO. During the escape trials all rats were able to find the hidden platform. With increasing number of trials the escape latency decreased in both groups. Latency times for the 4-VO rats were consistently longer than times for either the sham-operated or SA treated animals, as was the time to reach the platform region during the probe trial on day 6. Ischemic animals receiving SA took slightly longer to swim to the platform than sham operated animals, but performed just as well in the probe trial (Fig. 3). In the probe trials, rats after ischemia take longer than sham-operated rats. Thus prolongation of latency was markedly shortened by SA at a dose of 10 mg/kg.

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