七氟醚对血管痴呆性大鼠海马区细胞凋亡及Bcl-2蛋白表达的影响及相关机制研究

摘要 目的：探讨与研究七氟醚对血管性痴呆（Vascular dementia，VaD）大鼠海马区细胞凋亡及B淋巴细胞瘤-2(B-cell lymphoma-2，Bcl-2)蛋白表达的影响及相关机制。方法：60只老年雄性SD大鼠随机平分为两组-七氟醚与对照组，两组大鼠都采用双侧颈动脉缺血再灌注法制作VaD模型，七氟醚组与对照组在建模前分别吸入0.11 %七氟醚与空气各45 min，分别于建模后7 d、14 d与21 d进行Morris水迷宫实验检测大鼠的逃避潜伏期；建模后21 d，采用TUNEL法测定各组大鼠海马组织细胞凋亡情况，采用黄嘌呤氧化酶法、硫代巴比妥酸法分别测定血清超氧化物歧化酶（Superoxide dismutase，SOD）活性与丙二醛（Malondialdehyde，MDA）含量，采用Western blot法检测Bax、Bcl-2蛋白相对表达水平。结果：两组各有26只大鼠顺利建立VaD模型，建模后7 d、14 d与21 d，七氟醚组的逃避潜伏期均显著少于对照组(P<0.05)；建模后21 d，七氟醚组大鼠海马组织神经元细胞凋亡指数显著低于对照组(P<0.05)；建模后21 d，七氟醚组大鼠血清SOD活性显著高于对照组，而MDA含量则显著低于对照组(P<0.05)；建模后21 d，七氟醚组大鼠海马组织Bax、Bcl-2蛋白的相对表达水平均显著高于对照组(P<0.05)。结论：七氟醚干预可通过促进VaD大鼠海马组织抗凋亡蛋白Bcl-2表达抑制细胞凋亡，并可平衡大鼠的氧化应激反应水平，从而促进大鼠记忆功能恢复正常。

Effects of Sevoflurane on Apoptosis and Bcl-2 Protein Expression in Hippocampus of Rats with Vascular Dementia and Related Mechanisms

ABSTRACT Objective: To investigate and study the effects and related mechanism of sevoflurane on apoptosis of hippocampus and expression of B-cell lymphoma-2 (Bcl-2) protein in rats. Methods: 60 SD rats were randomly equally divided into two groups-sevoflurane and control group. Both groups of rats were made the vascular dementia model by bilateral carotid ischemia-reperfusion method. The sevoflurane group and control group were under construction Inhale 0.11% sevoflurane and air for 45 minutes before the mold, and the Morris water maze test was performed on 7 d, 14 d and 21 d after modeling to detect the escape latency of rats; 21 days after modeling, TUNEL method was used to determine the apoptosis of hippocampus in each group. Xanthine oxidase method and thiobarbituric acid method were used to determine serum superoxide dismutase (SOD) activity and malondialdehyde (MDA) content, respectively. Western blot was used to detect the relative expression levels of Bax and Bcl-2 proteins. Results: 26 rats in each group successfully established vascular dementia models. At 7 d, 14 d and 21 d after modeling, the escape latency of the sevoflurane group was significantly less than that of the control group(P<0.05); 21 days after modeling, the apoptosis index of neurons in the hippocampus of the sevoflurane group was significantly lower than that of the control group(P<0.05); 21 days after modeling, the serum SOD activity of rats in the sevoflurane group was significantly higher than that of the control group, while the MDA content was significantly lower than that of the control group (P<0.05); 21 days after modeling, the relative expression levels of Bax and Bcl-2 protein in hippocampus of rats in the sevoflurane group were significantly higher than those in the control group(P<0.05). Conclusion: Sevoflurane intervention can inhibit cell apoptosis by promoting the expression of the anti-apoptotic protein Bcl-2 in the hippocampus of VaD rats, and can balance the level of oxidative stress in rats, thereby promoting the normal memory function of rats.