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Protection of sodium ferulate on cerebral ischemic-reperfusion injury in rats after ischemic preconditioning / 中国组织工程研究
Chinese Journal of Tissue Engineering Research ; (53): 177-179, 2006.
Article in Chinese | WPRIM | ID: wpr-408536
ABSTRACT

BACKGROUND:

How to lessen neuronal necrosis to promote recovery of nerve function after ischemic cerebral injury? Cerebral ischemic preconditioning (IP) alleviates ischemic cerebral injury caused by re-ischemia to certain extent. It has been verified that sodium ferulate can lessen the incidence of neuron apoptosis after cerebral ischemia. Whether does sodium ferulate enhance the nerve protection of IP brain to not?

OBJECTIVE:

To explore the protection of sodium ferulate allied with IP in cerebral ischemic-reperfusion injury.

DESIGN:

Randomized controlled animal experiment was designed.

SETTING:

Neurological Surgery Department of 2nd Affiliated Hospital of Jiangxi Medical College, Department of Physiology of Jiangxi Medical College, Institute of Urinary Surgery of Jiangxi Medical College.MATERIALS The experiment was perforned in Laboratory Room of Neurological Surgery Department of 2nd affiliated Hospital of Jiangxi Medical College from May 2001 to April 2002, in which, 85 Wistar male rats were employed, mass weighted varied from 250-300 g.

METHODS:

The rats were randomized into 4 groups ① The control without ischemia (10 rats) Vertebral artery was ligatured bilaterally and common carotid artery was not clipped bilaterally. ② The control with ischemia (25 rats) Vertebral artery was ligatured bilaterally for 48 hours and common carotid artery was clipped for 10 minutes. ③ IP group (25rats) Vertebral artery was ligatured bilaterally for 48 hours and common carotid artery was clipped for 2 minutes, and 24 hours later, the common carotid artery was clipped again for another 10 minutes. ④ Sodium ferulate allied with IP group (Allied group) (24 rats) After IP, the common carotid artery was clipped again for 30 minutes and sodium ferulate (200 mg/kg)was injected intravenously from tail. The control without ischemia was subdivided into two groups of 2 days and 7 days after reperfusion respectively (5 rats for each one). The control with ischemia, IP group and allied group were subdivided into 5 groups of 6 bours, 12 hours, 24 hours,2 days and 7 days after reperfusion successively (5 rats for each one).The rats were sacrificed to collect brains at phase spots in each group.Coronary brain slice was collected 2.2 mm posterior to the optic chiasm and the effects of allied with was observed on neuron count and apoptotic cell count in cortex and hippocampal CA1 in cerebral ischemia reperfusion.MAIN OUTCOME

MEASURES:

Neuron count and apoptotic cell count in cortex and hippocampal CA1.

RESULTS:

Totally 85 experimental rats all entered result analysis. ①Neuron count in cerebral cortex and hippocampal CA1 On the 7th day after ischemia, the counts in IP group and allied group were higher than ischemia control (268±8.5, 244±12.5, 135±5.6, P < 0.01). ② Count of TUNEL positive cell in cerebral cortex and hippocampal CA1 The count in allied group was lower than that in IP group and ischemia control (12 hours1.2±0.8, 15.5±2.1, 39.8±3.9; 24 hours 1.8±1.6, 39.3±11.8, 191.3±19.1;2 days 2.8±1.2, 68.3±13.6, 328.4±24.0, P < 0.01), and that in IP group was lower than ischemic control (P < 0.01).

CONCLUSION:

IP lessens apoptotic neuron count in ischemic region.Sodium ferulate allied with IP further intensifies such effect and provides the protection of ischemic reperfusion injury of brain.
Full text: Available Index: WPRIM (Western Pacific) Type of study: Controlled clinical trial Language: Chinese Journal: Chinese Journal of Tissue Engineering Research Year: 2006 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Type of study: Controlled clinical trial Language: Chinese Journal: Chinese Journal of Tissue Engineering Research Year: 2006 Type: Article