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首页> 外文期刊>BMC Neuroscience >Isoliquiritigenin attenuates lipopolysaccharide-induced cognitive impairment through antioxidant and anti-inflammatory activity
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Isoliquiritigenin attenuates lipopolysaccharide-induced cognitive impairment through antioxidant and anti-inflammatory activity

机译：异寡糖原蛋白通过抗氧化剂和抗炎活性减轻脂多糖引起的认知障碍

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Oxidative stress and neuroinflammation are central pathogenic mechanisms common to many neurological diseases. Isoliquiritigenin (ISL) is a flavonoid in licorice with multiple pharmacological properties, including anti-inflammatory activity, and has demonstrated protective efficacy against acute neural injury. However, potential actions against cognitive impairments have not been examined extensively. We established a rat model of cognitive impairment by intracerebroventricular injection of lipopolysaccharide (LPS), and examined the effects of ISL pretreatment on cognitive function, hippocampal injury, and hippocampal expression of various synaptic proteins, antioxidant enzymes, pro-inflammatory cytokines, and signaling factors controlling anti-oxidant and pro-inflammatory responses. Rats receiving LPS alone demonstrated spatial learning deficits in the Morris water maze test as evidenced by longer average escape latency, fewer platform crossings, and shorter average time in the target quadrant than untreated controls. ISL pretreatment reversed these deficits as well as LPS-induced decreases in the hippocampal expression levels of synaptophysin, postsynaptic density-95, brain-derived neurotrophic factor, superoxide dismutase, glutathione peroxidase, and BCL-2. ISL pretreatment also reversed LPS-induced increases in TUNEL-positive (apoptotic) cells, BAX/BCL-2 ratio, and expression levels of tumor necrosis factor-α, interleukin (IL)-1β, IL-6, and C-C motif chemokine ligand 3. Pretreatment with ISL increased the expression levels of phosphorylated (p)-GSK-3β, nuclear NRF2, HO-1 mRNA, and NQO1 mRNA, and reversed LPS-induced nuclear translocation of nuclear factor (NF)-κB. ISL protects against LPS-induced cognitive impairment and neuronal injury by promoting or maintaining antioxidant capacity and suppressing neuroinflammation, likely through phosphorylation-dependent inactivation of GSK-3β, enhanced expression of NRF2-responsive antioxidant genes, and suppression of NF-κB-responsive pro-inflammatory genes.
机译：氧化应激和神经炎症是许多神经系统疾病共有的主要致病机制。异黄体生成素（ISL）是甘草中的一种类黄酮，具有多种药理特性，包括抗炎活性，并已显示出对急性神经损伤的保护作用。但是，尚未广泛研究针对认知障碍的潜在作用。我们建立了脑室内注射脂多糖（LPS）引起的认知障碍的大鼠模型，并研究了ISL预处理对各种突触蛋白，抗氧化酶，促炎性细胞因子和信号传导因子的认知功能，海马损伤和海马表达的影响控制抗氧化和促炎反应。与未治疗的对照组相比，仅接受LPS的大鼠在Morris水迷宫测试中表现出空间学习缺陷，这是由更长的平均逃逸潜伏期，更少的平台穿越和目标象限中的平均时间所证明的。 ISL预处理逆转了这些缺陷以及LPS诱导的海马突触素，突触后密度95，脑源性神经营养因子，超氧化物歧化酶，谷胱甘肽过氧化物酶和BCL-2的表达水平下降。 ISL预处理还逆转了LPS诱导的TUNEL阳性（凋亡）细胞，BAX / BCL-2比和肿瘤坏死因子-α，白介素（IL）-1β，IL-6和CC基序趋化因子配体的表达水平的增加3.用ISL预处理可增加磷酸化（p）-GSK-3β，核NRF2，HO-1 mRNA和NQO1 mRNA的表达水平，并逆转LPS诱导的核因子（NF）-κB核易位。 ISL通过促进或维持抗氧化能力并抑制神经炎症来预防LPS诱导的认知障碍和神经元损伤，这可能是通过GSK-3β的磷酸化依赖性失活，增强NRF2反应性抗氧化剂基因的表达以及抑制NF-κB反应性前体-炎症基因。

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