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Interventional therapy of advanced hepatocellular carcinoma(HCC) was constantly developing, and hepatic artery infusion chemotherapy (HAIC) had present significant therapeutic effect. With the update of chemotherapy drugs and compatibility, clinical research and application of HAIC for advanced HCC increased gradually. The main drugs and clinical progress of HAIC for advanced HCC were reviewed in this article.
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Objective To investigate the effect and the mechanism of parecoxib sodium pretreatment on permeability of blood-brain barrier in a rat model of focal cerebral ischemia-reperfusion injury.Methods Sixty male SD rats weighing 300g were randomly divided into 5 groups (n=12 each):sham operation group (group S);focal cerebral I/R group (group I/R);parecoxib sodium 5 mg/kg pretreatment group (group L);parecoxib sodium7.5mg/kg pretreatment group (group M);parecoxib sodium 10 mg/kg pretreatment group (group H) Middle cerebral artery occlusion models were made by reforming Longa suture method in SD rats.Thirty minutes before ischemia,rats in group L,M and H were injected with 5 mg/kg、7.5 mg/kg and 10 mg/kg parecoxib sodium through the internal jugular vein.Group S and group I/R received equal volume of normal saline.ELISA technique was used to determine the content of S100 β,TNF-α,IL-1 β in Plasma.The changes of cerebral water content and the Evans Blue exudation from brain capillaries were observed.Results Pretreated with parecoxib sodium (5mg/kg、7.5 mg/kg and 10 mg/kg),the content of S100 β,TNF-α,II-1 β in plasma were reduced.The cerebral water content and the EB in brain were reduced.Pretreated with parecoxib sodium 10 mg/kg,Longa scores were reduced.Conclusion Pretreatment with Parecoxib can protect blood-brain barrier against focal cerebral I/R injury by inhibition of the inflammatory reaetion.
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.