论文部分内容阅读
目的:观察加味桃核承气汤对β-淀粉样蛋白(Aβ)损伤大鼠学习记忆能力的影响,并探讨其作用机制。方法:SD大鼠随机分成3组,利用立体定位仪将Aβ1-42全长肽注射到大鼠双侧海马,构建Aβ损伤痴呆鼠模型(即Aβ1-42模型组);同时注射Aβ42-1反序列全长肽(即Aβ42-1对照组)和磷酸盐缓冲液(PBS)对照组(PBS对照组)。造模7 d后,每组再分成2个亚组,即加味桃核承气汤治疗组和空白组,分别以灌胃法(ig)给予加味桃核承气汤20 mL(20 g.kg-1)和同样体积的生理盐水,1次/d,连续21 d。利用水迷宫定位航行实验检测各组大鼠学习记忆能力情况,并应用Westen blotting方法检测各组大鼠海马组织中Tau,p-Tau蛋白的表达情况。结果:在定位航行实验中,Aβ1-42模型组大鼠平均逃避潜伏期(59.20±10.12)s长于Aβ42-1对照组(34.26±15.23)s和PBS对照组(32.07±9.50)s(P<0.05);Aβ1-42模型组大鼠应用加味桃核承气汤治疗后,平均逃避潜伏期明显缩短,与给予生理盐水组相比存在统计学差异(P<0.05);而应用加味桃核承气汤治疗后Aβ42-1对照组和PBS对照组的平均逃避潜伏期改变不明显。此外,应用加味桃核承气汤治疗的Aβ1-42模型组大鼠海马组织中Tau和p-Tau蛋白的表达水平也低于生理盐水组。结论:加味桃核承气汤可能通过降低脑组织中Tau蛋白表达,抑制Tau蛋白异常磷酸化,提高痴呆大鼠学习记忆能力。
Objective: To observe the effect of Modified Taohe Chengqi Decoction on learning and memory abilities of β-amyloid (Aβ) -induced injury in rats and its mechanism of action. Methods: The SD rats were randomly divided into three groups. Aβ1-42 full-length peptide was injected into bilateral hippocampus by stereotaxic apparatus to construct Aβ1-dendritic rat model (Aβ1-42 model group). At the same time, Aβ42-1 Sequence full-length peptide (ie Aβ42-1 control group) and phosphate buffered saline (PBS) control group (PBS control group). After 7 days of modeling, each group was further divided into 2 subgroups, that is, the modified Taohe Chengqi Decoction treatment group and the blank group were given 20ml (20g.kg -1) and the same volume of saline, 1 time / d, continuous 21 d. The learning and memory abilities of rats in each group were detected by water maze positioning navigation test. The expression of Tau and p-Tau protein in hippocampus were detected by Westen blotting. Results: In the navigation experiment, the mean escape latency of Aβ1-42 model rats was (59.20 ± 10.12) s longer than that of Aβ42-1 control group (34.26 ± 15.23) s and PBS control group (32.07 ± 9.50) s (P <0.05) ). The mean escape latency of Aβ1-42 model rats treated with Modified Taohe Chengqi Decoction was significantly shorter than that of saline control group (P <0.05). However, the application of Modified Taohe Chengqi Decoction After treatment, the average escape latency of Aβ42-1 control group and PBS control group was not obvious. In addition, the expression level of Tau and p-Tau protein in hippocampus of Aβ1-42 model group treated with Modified Taohe Chengqi Decoction was also lower than that of saline group. Conclusion: Modified Taohe Chengqi Decoction may improve the learning and memory ability of dementia rats by decreasing the expression of Tau protein in brain tissue, inhibiting the abnormal phosphorylation of Tau protein.