丹参酮提取物对阿尔茨海默病模型大鼠的干预效果及作用机制研究

李志海; 杨勤珍; 木崇仙

doi:10.13898/j.cnki.issn.1000-2200.2021.12.004

丹参酮提取物对阿尔茨海默病模型大鼠的干预效果及作用机制研究

Study on the intervention effects of tanshinone extract on Alzheimer's disease model rats and its mechanism

摘要

摘要:
目的探究丹参酮提取物对阿尔茨海默病模型大鼠的干预效果及作用机制。
方法选取40只SD健康雄性大鼠，随机选取10只作为正常组，其余30只建立阿尔兹海默病模型，并分为模型组、低剂量组、高剂量组。低剂量组、高剂量组大鼠分别使用10 g/L、30 g/L丹参酮提取物溶液进行灌胃，正常组、模型组大鼠使用0.9%氯化钠溶液进行灌胃。对各组大鼠学习记忆能力进行测试，酶联免疫吸附实验法检测白细胞介素（IL）-4、高敏C反应蛋白（hs-CRP）、肿瘤坏死因子-α（TNF-α）水平，流式细胞仪检测各组大鼠海马区细胞凋亡情况，Western blotting法检测Bcl-2、Bax、caspase-3表达。
结果模型组逃避潜伏期长于正常组（P < 0.01），穿越平台次数低于正常组（P < 0.01）；高剂量组大鼠逃避潜伏期低于模型组和低剂量组（P < 0.01），穿越平台次数多于模型组和低剂量组（P < 0.01和P < 0.05）。hs-CRP、TNF-α、IL-4水平由高到低的排序依次均为：模型组、高剂量组、低剂量组和正常组（P < 0.01）。4组之间不同时间点海马区细胞凋亡率由高到低的排序依次为：模型组、低剂量组、高剂量组和正常组（P < 0.01）。Bcl-2的表达量在4组之间由高到低的排序依次为：正常组、高剂量组、低剂量组和模型组（P < 0.01）；Bax与caspase-3的表达量在4组之间由高到低的排序依次均为：模型组、低剂量组、高剂量组和正常组（P < 0.01）。
结论使用丹参酮提取物对阿尔兹海默病模型大鼠进行干预，能够提升阿尔兹海默病大鼠学习记忆能力，减轻脑组织炎症反应，调控细胞凋亡相关蛋白Bcl-2、Bax、caspase-3相对表达量，抑制阿尔兹海默病大鼠海马区细胞凋亡，具有一定神经元保护作用。

Abstract:
ObjectiveTo explore the intervention effects of tanshinone extract on Alzheimer's disease model rats and its mechanism.
MethodsForty healthy male SD rats were randomly divided into the normal group, model group, low-dose group and high-dose group(10 rats in each group).The low-dose group and high-dose group were given 10 g/L and 30 g/L tanshinone extract by intragastric administration, respectively.The normal group and model group were given 0.9% sodium chloride solution by intragastric administration.The learning and memory ability in each group were tested.The levels of interleukin4(IL-4), high-sensitivity C-reactive protein(hs-CRP) and tumor necrosis factor-α(TNF-α) were detected using enzyme-linked immunosorbent assay, the apoptosis of hippocampal cells in each group was detected using flow cytometry, and the protein expression levels of Bcl-2, Bax and caspase-3 were detected using Western blotting.
ResultsThe latency of escape in model group was longer than that in normal group(P < 0.01), and the number of crossing platform in model group was lower than that in normal group(P < 0.01).The escape latency in high-dose group was lower than that in model group and low-dose group(P < 0.01), and the number of crossing platform in high-dose group was more than that in model group and low-dose group(P < 0.01 and P < 0.05).The order of hs-CRP, TNF-α and IL-4 levels from high to low was as follows: model group, high-dose group, low-dose group and normal group(P < 0.01).The order of apoptosis rate of hippocampal cells at different time points was as follows: model group, low-dose group, high-dose group and normal group(P < 0.01).The order of Bcl-2 expression in the four groups from high to low was the normal group, high-dose group, low-dose group and model group(P < 0.01).The expression levels of Bax and caspase-3 were in descending order among the four groups: model group, low-dose group, high-dose group and normal group(P < 0.01).
ConclusionsThe intervention of tanshinone extract on Alzheimer's disease model rats can improve the learning and memory ability, alleviate the inflammatory reaction of brain tissue, regulate the relative expression of apoptosis-related proteins, Bcl-2, Bax and caspase-3, and inhibit the apoptosis of hippocampal cells, which has certain neuronal protection effect in Alzheimer's disease rats.

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