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Effect of anti-dementia drugs on LPS induced neuroinflammation in mice.

机译:抗痴呆药对LPS诱导的小鼠神经炎症的作用。

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Inflammation has been recently implicated in pathogenesis of dementia disorders. Effect of anti-dementia (Acetylcholinesterase inhibitor) drugs tacrine, rivastigmine and donepezil were studied on neuroinflammation induced by intraperitoneal administration of lipopolysaccharide (LPS) in mice. Interleukin-2 (IL-2) and isoforms of acetylcholinesterase (AChE) were estimated in different brain areas as marker for neuroinflammation and cholinergic activity respectively. LPS significantly increased the level of IL-2 in all the brain areas while enhancement of AChE activity varied in brain areas. It was found that administration of tacrine, rivastigmine and donepezil in mice significantly attenuated the LPS induced increased levels of IL-2 along with the significant reduction of AChE activity predominantly in salt soluble (SS) fraction as compared to the detergent soluble (DS) fraction in a dose dependent manner. In vitro effect of LPS was also studied in different brain areas. LPS significantly increased the AChE activity in SS fractions but the significant increase was not found in DS fractions. The present study indicate that cholinesterase inhibitor anti-dementia drugs are effective against LPS induced neuroinflammation that may be linked to enhanced cholinergic activity.
机译:炎症最近与痴呆症的发病机理有关。研究了抗痴呆(乙酰胆碱酯酶抑制剂)药物他克林,卡巴拉汀和多奈哌齐对小鼠腹腔注射脂多糖(LPS)引起的神经炎症的作用。估计在不同的大脑区域中,白介素2(IL-2)和乙酰胆碱酯酶(AChE)的同工型分别作为神经炎症和胆碱能活性的标志。 LPS显着增加了所有脑区域的IL-2水平,而AChE活性的增强在脑区域有所不同。已发现在小鼠中施用他克林,卡巴拉汀和多奈哌齐显着减弱了脂多糖诱导的IL-2水平升高,并且与去污剂可溶性(DS)组分相比,主要是盐溶性(SS)组分的AChE活性显着降低。以剂量依赖的方式。还研究了在不同大脑区域中LPS的体外作用。 LPS显着增加了SS馏分中的AChE活性,但在DS馏分中未发现显着增加。本研究表明胆碱酯酶抑制剂抗痴呆药可有效抵抗LPS诱导的神经炎症,这可能与胆碱能活性增强有关。

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