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瑞士乳杆菌 KLDS1.8701 通过调节 Nrf-2 和肠道微生物群缓解 D-半乳糖诱导的衰老。

Lactobacillus helveticus KLDS1.8701 alleviates d-galactose-induced aging by regulating Nrf-2 and gut microbiota in mice.

机构信息

Key Laboratory of Dairy Science, Ministry of Education, Northeast Agricultural University, Harbin 150030, China.

出版信息

Food Funct. 2018 Dec 13;9(12):6586-6598. doi: 10.1039/c8fo01768a.


DOI:10.1039/c8fo01768a
PMID:30488048
Abstract

Aging is commonly associated with chronic oxidative stress and mild inflammation that can cause a variety of degenerative diseases. Lactic acid bacteria (LAB) provide several health benefits to the host including antioxidant activity and immune system regulation. However, there is a lack of information regarding the antioxidant mechanisms of probiotics in vivo. Therefore, the aim of this study was to elucidate the possible mechanisms for the preventive effect of LAB on aging. First, 25 LAB strains were screened for finding potential probiotics with high antioxidant capacity using in vitro methods. Second, d-galactose was administered by subcutaneous injection once daily for 8 weeks to establish an aging mouse model to investigate the protective effects and underlying mechanisms of the potential probiotic strain Lactobacillus helveticus KLDS1.8701, identified from the screening. The results in vitro showed that L. helveticus KLDS1.8701 had a better property with remarkable free radical scavenging activity. In vivo, L. helveticus KLDS1.8701 supplementation significantly ameliorated aging-related changes such as decreased organic index, liver injury and increased endotoxin. L. helveticus KLDS1.8701 supplementation reduced hepatic oxidative stress by modulating the Nrf-2 pathway. Notably, L. helveticus KLDS1.8701 supplementation restored the gut microbiota composition to that of the control group, resulting in increased butyrate production and decreased endotoxin production. These findings indicated that L. helveticus KLDS1.8701 supplementation manipulated gut microbiota and its metabolites could attenuate hepatic oxidative stress via the gut-liver axis.

摘要

衰老是与慢性氧化应激和轻度炎症相关的,这些因素会导致各种退行性疾病。乳酸菌(LAB)为宿主提供多种健康益处,包括抗氧化活性和免疫系统调节。然而,关于益生菌在体内的抗氧化机制的信息还很缺乏。因此,本研究旨在阐明 LAB 预防衰老的可能机制。首先,使用体外方法筛选了 25 株 LAB 菌株,以寻找具有高抗氧化能力的潜在益生菌。其次,通过皮下注射每天一次给予 D-半乳糖 8 周,建立衰老小鼠模型,以研究从筛选中鉴定出的潜在益生菌菌株瑞士乳杆菌 KLDS1.8701 的保护作用及其潜在机制。体外结果表明,瑞士乳杆菌 KLDS1.8701 具有更好的特性,具有显著的自由基清除活性。在体内,瑞士乳杆菌 KLDS1.8701 补充显著改善了与衰老相关的变化,如有机指数降低、肝损伤和内毒素增加。瑞士乳杆菌 KLDS1.8701 通过调节 Nrf-2 通路减轻肝氧化应激。值得注意的是,瑞士乳杆菌 KLDS1.8701 补充恢复了肠道微生物群落组成,使丁酸产生增加,内毒素产生减少。这些发现表明,瑞士乳杆菌 KLDS1.8701 通过操纵肠道微生物群及其代谢物,通过肠道-肝脏轴减轻肝氧化应激。

相似文献

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Lactobacillus helveticus KLDS1.8701 alleviates d-galactose-induced aging by regulating Nrf-2 and gut microbiota in mice.

Food Funct. 2018-12-13

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[10]
The molecular mechanisms of probiotic strains in improving ageing bone and muscle of d-galactose-induced ageing rats.

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