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目的:观察灯盏乙素对痴呆模型大鼠脑组织中几种炎性因子表达的影响,探讨其可能的抗炎治疗机制。方法:Wistar大鼠42只,随机分为5组,正常对照组、假手术组、学习记忆损伤模型组、灯盏乙素处理组和脑复康处理组。用双侧脑室注射β淀粉样蛋白(Aβ25-35)联合ip D-半乳糖方法建立痴呆大鼠模型;造模后次日分别用28 mg.kg-1灯盏乙素和365 mg.kg-1脑复康连续ig 20 d;实时定量聚合酶链法(RT-PCR)测定大鼠脑组织核因子(nuclear factor,NF)-κB p65表达的变化;免疫组织化学方法检测大鼠脑组织白介素-1β(IL-1β),白介素-6(IL-6)及肿瘤坏死因子-α(TNF-α)的表达。结果:与正常组和假手术组相比,模型组大鼠脑组织中NF-κB p65 mRNA表达水平上升了27%和31%(P<0.05),IL-1β,IL-6,TNF-α表达的阳性细胞分值正常组(1.3±0.5,1.6±0.5,1.6±0.69)和假手术组(1.5±0.5,1.6±0.7,2.0±0.7)。模型组明显上升(2.9±0.7,3.2±0.8,3.0±0.82),P<0.05。灯盏乙素处理后NF-κB p65的mRNA表达水平下调了20%(P<0.05),IL-1β,IL-6和TNF-α表达的阳性细胞分值明显下降(2.1±0.67,2.3±0.70,2.2±0.53),P<0.05。结论:灯盏乙素可阻断痴呆大鼠脑组织中NF-κB p65的活化,抑制炎性因子释放,改善学习记忆能力,通过减轻神经炎症损伤起到神经保护的作用。
Objective: To observe the effect of scutellarin on the expression of several inflammatory cytokines in the brain of dementia model rats and to explore its possible anti-inflammatory treatment mechanism. Methods: Forty-two Wistar rats were randomly divided into 5 groups: normal control group, sham operation group, learning and memory injury model group, scutellarin treatment group and naofukang treatment group. The rat model of dementia was established by bilateral intracerebroventricular injection of amyloid beta (Aβ25-35) and ip D-galactose. The day after the model was treated with 28 mg.kg-1 scutellarin and 365 mg.kg-1 Nao Fukang continuous ig 20 d; real-time quantitative polymerase chain reaction (RT-PCR) determination of rat brain tissue nuclear factor (nuclear factor, NF-κB p65 expression changes; immunohistochemical detection of rat brain tissue interleukin- IL-1β, IL-6 and TNF-α were measured by ELISA. Results: Compared with normal group and sham operation group, the expression of NF-κB p65 mRNA increased by 27% and 31% (P <0.05), while the expression of IL-1β, IL-6 and TNF- Positive cells expressed in normal group (1.3 ± 0.5, 1.6 ± 0.5, 1.6 ± 0.69) and sham group (1.5 ± 0.5, 1.6 ± 0.7, 2.0 ± 0.7). The model group increased significantly (2.9 ± 0.7, 3.2 ± 0.8, 3.0 ± 0.82), P <0.05. The expression of NF-κB p65 mRNA was down-regulated by 20% (P <0.05) after treatment with Scutellarin. The positive cells of IL-1β, IL-6 and TNF-α were significantly decreased (2.1 ± 0.67,2.3 ± 0.70 , 2.2 ± 0.53), P <0.05. Conclusion: Scutellarin can block the activation of NF-κB p65 in brain tissue of dementia rats, inhibit the release of inflammatory cytokines, improve the ability of learning and memory, and play a neuroprotective role by reducing the damage of neuroinflammation.