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PS23 可延缓衰老加速敏感 8 号小鼠(SAMP8)与年龄相关的认知能力下降的进展。

PS23 Delays Progression of Age-Related Cognitive Decline in Senescence Accelerated Mouse Prone 8 (SAMP8) Mice.

机构信息

Graduate Institute of Metabolism and Obesity Sciences, Taipei Medical University, Taipei 11031, Taiwan.

Department of Food Science, Nutrition, and Nutraceutical Biotechnology, Shih Chien University, Taipei 10462, Taiwan.

出版信息

Nutrients. 2018 Jul 12;10(7):894. doi: 10.3390/nu10070894.

DOI:10.3390/nu10070894
PMID:30002347
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6073302/
Abstract

Probiotic supplements are potential therapeutic agents for age-related disorders due to their antioxidant and anti-inflammatory properties. However, the effect of probiotics on age-related brain dysfunction remains unclear. To investigate the effects of PS23 (LPPS23) on the progression of age-related cognitive decline, male and female senescence-accelerated mouse prone 8 (SAMP8) mice were divided into two groups ( = 6 each): the control and PS23 groups. From the age of 16 weeks, these groups were given saline and LPPS23, respectively, because SAMP8 mice start aging rapidly after four months of age. After 12 weeks of treatment, we evaluated the effect of LPPS23 by analyzing their appearance, behavior, neural monoamines, anti-oxidative enzymes, and inflammatory cytokines. The PS23 group showed lower scores of senescence and less serious anxiety-like behaviors and memory impairment compared to the control group. The control mice also showed lower levels of neural monoamines in the striatum, hippocampus, and serum. Moreover, LPPS23 induced the anti-oxidative enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPx). Higher levels of tumor necrosis factor (TNF)-α and monocyte chemotactic protein-1 (MCP1) and lower levels of interleukin (IL)-10 indicated that LPPS23 modulated the inflammation. Our results suggest that LPPS23 supplements could delay age-related cognitive decline, possibly by preventing oxidation and inflammation and modulating gut⁻brain axis communication.

摘要

益生菌补充剂具有抗氧化和抗炎特性,因此可能成为与年龄相关疾病的治疗药物。然而,益生菌对与年龄相关的大脑功能障碍的影响尚不清楚。为了研究 PS23(LPPS23)对与年龄相关的认知能力下降进展的影响,雄性和雌性快速衰老性淀粉样蛋白前体(SAMP8)小鼠被分为两组(每组 6 只):对照组和 PS23 组。从 16 周龄开始,这两组分别给予生理盐水和 LPPS23,因为 SAMP8 小鼠在四个月后开始迅速衰老。经过 12 周的治疗,我们通过分析外观、行为、神经单胺、抗氧化酶和炎症细胞因子来评估 LPPS23 的效果。与对照组相比,PS23 组的衰老评分较低,焦虑样行为和记忆障碍较轻。对照组的纹状体、海马体和血清中的神经单胺水平也较低。此外,LPPS23 诱导了超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GPx)等抗氧化酶。肿瘤坏死因子(TNF)-α和单核细胞趋化蛋白-1(MCP1)水平升高,白细胞介素(IL)-10 水平降低,表明 LPPS23 调节了炎症。我们的结果表明,LPPS23 补充剂可能通过预防氧化和炎症以及调节肠道-大脑轴通讯来延缓与年龄相关的认知能力下降。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ca8/6073302/09f22e7138d8/nutrients-10-00894-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ca8/6073302/165728487069/nutrients-10-00894-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ca8/6073302/29c37ccd9aa1/nutrients-10-00894-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ca8/6073302/c86cde4aa2eb/nutrients-10-00894-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ca8/6073302/bf0a7a1c2658/nutrients-10-00894-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ca8/6073302/e9a07276b39c/nutrients-10-00894-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ca8/6073302/09f22e7138d8/nutrients-10-00894-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ca8/6073302/165728487069/nutrients-10-00894-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ca8/6073302/29c37ccd9aa1/nutrients-10-00894-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ca8/6073302/c86cde4aa2eb/nutrients-10-00894-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ca8/6073302/bf0a7a1c2658/nutrients-10-00894-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ca8/6073302/e9a07276b39c/nutrients-10-00894-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ca8/6073302/09f22e7138d8/nutrients-10-00894-g006.jpg

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