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热灭活乳酸乳球菌KC24改善东莨菪碱诱导的ICR小鼠记忆损伤。

Heat-Killed Lactococcus Lactis KC24 Ameliorates Scopolamine-Induced Memory Impairment in ICR Mice.

作者信息

Lee Na-Kyoung, Lee Yunjung, Park Ji Ye, Park Eunju, Paik Hyun-Dong

机构信息

Department of Food Science and Biotechnology of Animal Resources, Konkuk University, Seoul, 05029, Korea.

Department of Food and Nutrition, Kyungnam University, Changwon, 51767, Korea.

出版信息

Probiotics Antimicrob Proteins. 2024 Jun 19. doi: 10.1007/s12602-024-10268-6.

Abstract

Heat-killed Lactococcus lactis KC24 (H-KC24) has been examined for its neuroprotective effects in SH-SY5Y cells. We hypothesized that H-KC24 could alleviate memory impairment through the gut-brain axis. Scopolamine (1 mg/kg/day) was administered to ICR mice to induce memory impairment. Low- and high-dose H-KC24 cells (1 × 10 and 2 × 10 CFU/day, respectively) or donepezil (DO, 2 mg/kg) were administered for 14 days. H-KC24 treatment alleviated the deleterious scopolamine-induced memory effects on the recognition index and object recognition ability in the novel object recognition test and the Y-maze test. Changes in neurotransmitters and synaptic plasticity were confirmed by measuring acetylcholine, acetylcholinesterase, choline acetyltransferase, brain-derived neurotrophic factor, cyclic AMP response element-binding protein, and phosphorylated cyclic AMP response element-binding protein expression in brain tissues. In the H-KC24 and DO groups, β-secretase levels increased, whereas amyloid β levels decreased, demonstrating that H-KC24 can improve memory impairment caused by oxidative stress. This study demonstrated the positive effects of H-KC24 in a scopolamine-induced memory impairment mouse model.

摘要

已对热灭活的乳酸乳球菌KC24(H-KC24)在SH-SY5Y细胞中的神经保护作用进行了研究。我们假设H-KC24可以通过肠-脑轴减轻记忆障碍。向ICR小鼠注射东莨菪碱(1毫克/千克/天)以诱导记忆障碍。分别给予低剂量和高剂量的H-KC24细胞(分别为1×10和2×10 CFU/天)或多奈哌齐(DO,2毫克/千克),持续14天。在新物体识别试验和Y迷宫试验中,H-KC24治疗减轻了东莨菪碱诱导的对识别指数和物体识别能力的有害记忆效应。通过测量脑组织中乙酰胆碱、乙酰胆碱酯酶、胆碱乙酰转移酶、脑源性神经营养因子、环磷酸腺苷反应元件结合蛋白和磷酸化环磷酸腺苷反应元件结合蛋白的表达,证实了神经递质和突触可塑性的变化。在H-KC24和DO组中,β-分泌酶水平升高,而淀粉样β水平降低,表明H-KC24可以改善由氧化应激引起的记忆障碍。本研究证明了H-KC24在东莨菪碱诱导的记忆障碍小鼠模型中的积极作用。

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