摘要
目的观察不同剂量羟丁酸钠对缺血缺氧性脑损伤(HIBD)新生大鼠大脑皮层Bcl-2、 Bax蛋白表达的影响。方法新生7d SD大鼠,随机分为假手术组(S组)、生理盐水对照组(C组)和羟丁酸钠组(γ1、γ2、γ3组),每组又分为5个亚组,分别为缺血缺氧(HI)后1 h、3 h、1 d、3 d、7 d(n=6)。按Rice法制作HIBD模型。C、γ1、γ2和γ3组分别在HI后即刻腹腔注射生理盐水0．2 ml/10 g、羟丁酸钠50、100、200 mg／kg,3次／日。免疫组化方法检测HI后各时间点大脑皮层Bcl-2、Bax蛋白表达。结果与S组比较,C、γ1、γ2、γ3组Bcl-2及Bax蛋白表达在HI后1、3 h即增高,HI后1 d达到高峰,HI后3 d下降(P<0．05),HI后7d时基本恢复正常;与C、γ3比较,HI后1、3 d时γ1、γ2组Bcl-2蛋白表达增高,Bax蛋白表达降低(P<0．05);γ3组与C组间Bcl-2、Bax蛋白表达比较差异无统计学意义(P> 0．05)。结论羟丁酸钠上调HIBD新生大鼠大脑皮层Bcl-2蛋白表达,下调Bax蛋白表达。
Objective To investigate the effects of sodium hydroxybutyrate （γ-OH） on the expression of Bcl-2 and Bax in cerebral cortex induced by hypoxic-ischemic brain injury （HIBI）.Methods 7-day-old SD rats weighing 12.0-16.0 g were randomized into 5 groups： sham operation group; HIBI group and 3 γ-OH groups which received intraperitoneal γ-OH 50, 100 or 200 mg· kg^-1 3 times a day for a maximum of 7 days immediately after HIBI. HIBI was produced by left common carotid artery hgation followed by 2 h hypoxic air （8% 02） inhalation. The animals were killed at 1 h, 3 h, 1 d, 3 d and 7 d （ n = 6 each） after HIBI and their brains were removed for detection of Bcl-2 and Bax expression in the left cerebral cortex using immuno-histochemical staining. Results The expression of Bcl-2 and Bax in cerebral cortex was significantly increased at 1 h and 3 h after HIBI and peaked at 1 d and returned to the normal level at 7 d in HIBI and 3 γ-OH groups as compared to the sham operation group. The Bcl-2 expression was significantly higher while Bax expression significantly lower at 1 d and 3 d after HIBI in group γ-OH 1 and 2 than in group HIBI. There was no significant difference in Bcl-2 and Bax expression between group HIBI and γ-OH 3. Conclusion Sodium hydroxybutyrate upregulates Bcl-2 expression and dowm＇egulates Bax expression in cerebral cortex induced by HIBI.
出处
《中华麻醉学杂志》
CAS
CSCD
北大核心
2006年第3期249-251,共3页
Chinese Journal of Anesthesiology
基金
江苏省卫生厅医学科技发展基金资助项目(Z200306)
关键词
羟丁酸钠
脑缺氧缺血
脑损伤
细胞凋亡易感蛋白
大脑皮质
Sodium oxybate
Hypexic-ischemic, brain
Brain injury
Cellular apoptusis susceptibility protein
Cerebral cortex
