2010Zhonghua mazuixue zazhiRequires access

Effect of parecoxib pretreatment on focal cerebral ischemia-reperfusion injury in rats

Shaoxing Liu, Danyan Liu, Huisheng Wu, Min An

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Abstract

Objective To investigate the effect of parecoxib pretreatment on focal cerebral ischemia-reperfusion (I/R) injury in rats. Methods Sixty-four male SD rats weighing 250-300 g were randomly divided into 4 groups ( n= 16 each): sham operation group (group S); focal cerebral I/R group; focal cerebral I/R + parecoxib 5 mg/kg group (group P5); focal cerebral I/R + parecoxib 10 mg/kg group (group P10). Focal cerebral I/R was produced by occlusion of middle cerebral artery for 2 h followed by 24 h of reperfusion. Parecoxib 5 and 10 mg/kg were injected intravenously through the internal jugular vein 30 min before ischemia in group P5 and P10 respectively. The neurologic deficit scores (NDSs) were measured at 24 h of reperfusion and then the rats were decapitated.Brains were rapidly removed for determination of the infarct volume, apoptosis rate and expression of Bcl-2 and Bax. The ratio of Bcl-2 to Bax (Bcl-2/Bax) was calculated. Results The NDSs, apoptosis rate and expression of Bcl-2 and Bax were significantly higher, Bcl-2/Bax was significantly lower, and the infarct volume was significantly larger in group I/R than in group S ( P < 0.01 ). The NDSs were significantly lower in group P10, and the apoptosis rate and Bax expression were significantly lower, the infarct volume was significantly smaller, Bcl-2 expression and Bcl-2/Bax were significantly higher in group P5 and P10 than in group I/R (P <0.05 or 0.01). The infarct volume was significantly smaller, the apoptosis rate and Bax expression were significantly lower, and Bcl-2 expression and Bcl-2/Bax were significantly higher in group P10 than in group P5 ( P < 0.05 or 0.01 ). Conclusion Pretreatment with parecoxib can attenuate focal cerebral I/R injury in a dose-dependent manner through inhibition of cell apoptosis via up-regulation of Bcl-2 expression and down-regulation of Bax expression in rats. Key words: Cyclooxygenase 2 inhibitors; Brain; Reperfusion injury

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Objective To investigate the effect of parecoxib pretreatment on focal cerebral ischemia-reperfusion (I/R) injury in rats. Methods Sixty-four male SD rats weighing 250-300 g were randomly divided into 4 groups ( n= 16 each): sham operation group (group S); focal cerebral I/R group; focal cerebral I/R + parecoxib 5 mg/kg group (group P5); focal cerebral I/R + parecoxib 10 mg/kg group (group P10). Focal cerebral I/R was produced by occlusion of middle cerebral artery for 2 h followed by 24 h of reperfusion. Parecoxib 5 and 10 mg/kg were injected intravenously through the internal jugular vein 30 min before ischemia in group P5 and P10 respectively. The neurologic deficit scores (NDSs) were measured at 24 h of reperfusion and then the rats were decapitated.Brains were rapidly removed for determination of the infarct volume, apoptosis rate and expression of Bcl-2 and Bax. The ratio of Bcl-2 to Bax (Bcl-2/Bax) was calculated. Results The NDSs, apoptosis rate and expression of Bcl-2 and Bax were significantly higher, Bcl-2/Bax was significantly lower, and the infarct volume was significantly larger in group I/R than in group S ( P < 0.01 ). The NDSs were significantly lower in group P10, and the apoptosis rate and Bax expression were significantly lower, the infarct volume was significantly smaller, Bcl-2 expression and Bcl-2/Bax were significantly higher in group P5 and P10 than in group I/R (P <0.05 or 0.01). The infarct volume was significantly smaller, the apoptosis rate and Bax expression were significantly lower, and Bcl-2 expression and Bcl-2/Bax were significantly higher in group P10 than in group P5 ( P < 0.05 or 0.01 ). Conclusion Pretreatment with parecoxib can attenuate focal cerebral I/R injury in a dose-dependent manner through inhibition of cell apoptosis via up-regulation of Bcl-2 expression and down-regulation of Bax expression in rats. Key words: Cyclooxygenase 2 inhibitors; Brain; Reperfusion injury

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Available abstract

Objective To investigate the effect of parecoxib pretreatment on focal cerebral ischemia-reperfusion (I/R) injury in rats. Methods Sixty-four male SD rats weighing 250-300 g were randomly divided into 4 groups ( n= 16 each): sham operation group (group S); focal cerebral I/R group; focal cerebral I/R + parecoxib 5 mg/kg group (group P5); focal cerebral I/R + parecoxib 10 mg/kg group (group P10). Focal cerebral I/R was produced by occlusion of middle cerebral artery for 2 h followed by 24 h of reperfusion. Parecoxib 5 and 10 mg/kg were injected intravenously through the internal jugular vein 30 min before ischemia in group P5 and P10 respectively. The neurologic deficit scores (NDSs) were measured at 24 h of reperfusion and then the rats were decapitated.Brains were rapidly removed for determination of the infarct volume, apoptosis rate and expression of Bcl-2 and Bax. The ratio of Bcl-2 to Bax (Bcl-2/Bax) was calculated. Results The NDSs, apoptosis rate and expression of Bcl-2 and Bax were significantly higher, Bcl-2/Bax was significantly lower, and the infarct volume was significantly larger in group I/R than in group S ( P < 0.01 ). The NDSs were significantly lower in group P10, and the apoptosis rate and Bax expression were significantly lower, the infarct volume was significantly smaller, Bcl-2 expression and Bcl-2/Bax were significantly higher in group P5 and P10 than in group I/R (P <0.05 or 0.01). The infarct volume was significantly smaller, the apoptosis rate and Bax expression were significantly lower, and Bcl-2 expression and Bcl-2/Bax were significantly higher in group P10 than in group P5 ( P < 0.05 or 0.01 ). Conclusion Pretreatment with parecoxib can attenuate focal cerebral I/R injury in a dose-dependent manner through inhibition of cell apoptosis via up-regulation of Bcl-2 expression and down-regulation of Bax expression in rats. Key words: Cyclooxygenase 2 inhibitors; Brain; Reperfusion injury

Key concepts: Parecoxib, Apoptosis, Ischemia, Medicine, Anesthesia, Reperfusion injury, Middle cerebral artery, Cerebral infarction

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