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对脂多糖诱导大鼠记忆障碍的预防作用。

Preventive Effect of on Memory Impairment Induced by Lipopolysaccharide in Rats.

机构信息

Department of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran 19839-63113, Iran.

Department of Clinical Biochemistry, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah 6715847141, Iran.

出版信息

ACS Chem Neurosci. 2022 Nov 16;13(22):3180-3187. doi: 10.1021/acschemneuro.2c00500. Epub 2022 Nov 1.

Abstract

Recent studies have indicated that dysfunction of gut microbiota, living microorganisms of the digestive tract, plays a role in the pathogenesis of neurodegenerative disorders, indicating the valuable impact of probiotics as a potential preventive or therapeutic strategy. is a yeast probiotic with beneficial effects on various disorders, ranging from inflammatory gastrointestinal diseases to brain and behavioral disorders. Herein, we examined the effect of on memory impairment induced by lipopolysaccharide (LPS) in Wistar rats. Four groups of rats were used in this study ( = 10): (1) control [Cnt], (2) LPS, (3) LPS + [LPS + S], and (4) [S]. Animals were orally administered (250 mg/rat) or saline by gavage for 4 weeks. From the 14th day of the study, animals were administered intraperitoneal LPS (0.25 mg/kg/day) or saline for 9 days. We assessed memory impairment, neuroinflammation, and amyloid-β deposition. ameliorated LPS-induced memory dysfunction. We observed that significantly reduced the elevated levels of serum interleukin (IL)-1β, IL-6, and tumor necrosis factor-α, as well as hippocampal levels of NLRP3 and caspase-1 in the LPS model. Moreover, alleviated amyloid-β deposition in the rat hippocampus. Collectively, our findings indicated that could inhibit memory impairment, neuroinflammation, and amyloid-β accumulation induced by LPS, possibly by modifying the gut microbiota.

摘要

最近的研究表明,肠道微生物群落(消化道中的微生物群)功能障碍在神经退行性疾病的发病机制中起作用,这表明益生菌作为一种潜在的预防或治疗策略具有重要意义。 是一种酵母益生菌,对各种疾病都有有益的影响,从炎症性胃肠道疾病到大脑和行为障碍。在此,我们研究了 对脂多糖(LPS)诱导的 Wistar 大鼠记忆障碍的影响。本研究使用了四组大鼠(n = 10):(1)对照组[Cnt],(2)LPS 组,(3)LPS + 组[LPS + S],和(4) 组[S]。动物通过灌胃口服给予 (250 mg/大鼠)或生理盐水 4 周。从研究的第 14 天开始,动物每天腹腔内注射 LPS(0.25 mg/kg)或生理盐水 9 天。我们评估了记忆障碍、神经炎症和淀粉样蛋白-β沉积。 改善了 LPS 诱导的记忆功能障碍。我们观察到 显著降低了 LPS 模型中血清白细胞介素(IL)-1β、IL-6 和肿瘤坏死因子-α以及海马 NLRP3 和半胱天冬酶-1水平的升高。此外, 减轻了大鼠海马中的淀粉样蛋白-β沉积。总之,我们的研究结果表明, 通过调节肠道微生物群, 可以抑制 LPS 诱导的记忆障碍、神经炎症和淀粉样蛋白-β积累。

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