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Studies on Bioactivity and Molecular Mechanism of Bifidobacterium longum on Anti-aging in Caenorhabditis elegans

菅原, 賢也 筑波大学 DOI:10.15068/0002001041

2021.08.17

概要

In modern society, human life expectancy is increasing compared to the past, and the term "health span" is beginning to be used in addition to the term "life span". Although currently there is a gap between life span and health span, reducing the gap by extending health span is important to improve people's quality of life. In this study, I analyzed the effects of bifidobacterium on health and anti-aging as candidates for bioactive substances that can extend health span. In this study, Caenorhabditis elegans was used as an experimental model organism.

Bifidobacterium is a probiotics, which are beneficial microorganisms to humans, and is the highest percentage of probiotics in the human gut. As such, they have considerable influence on the host and have beneficial effects on human health, including improvement of intestinal flora. Currently, various physiological effects of bifidobacterium are known to enhance immune function, alleviate allergies, and inhibit cancer development. Although its physiological effects on anti-aging have also been reported, there are many unresolved aspects of its effects, which I sought to elucidate in this study.

C. elegans is widely used as a model organism for biological experiments because it is easy to breed. In addition, it has basic organs such as the intestines, nerves, and reproductive organs, which enable it to simulate the digestion and absorption of food extracts and functional substances.

Although several previous studies have analyzed the bioactive effects of bifidobacterium using nematodes, there are only a few studies on anti-aging and there are many unexplored aspects. In this study, I fed sterilized Bifidobacterium longum (BR-108, BL) together with E. coli, the food source of nematodes, in order to explore a new bioactive effect of B. longum on anti-aging and to elucidate the mechanism of its action.

C. elegans fed a mixture of BL and E. coli increased various stress tolerance compared to C. elegans fed only E. coli. BL increased the expression of genes related to stress tolerance, which in turn increased the stress tolerance, extended the lifespan and prevented the loss of motility with aging. I also measured muscle mass, ATP levels, mitochondrial mass and mitochondrial membrane potential, and ROS levels in nematodes for further analysis of the significant suppression of age-related motility loss and found that BL-induced change of these phenotypes were upregulated. It was suggested that the maintenance of motility was caused by the effects on muscle and mitochondria. Compared to BL-induced changes in muscle mass, mitochondrial mass and membrane potential were substantially increased. Therefore, I hypothesized that BL has a greater effect on mitochondria, which produce ATP for muscle energy, than on muscle, and I used mitochondrial complex inhibitors to search for mitochondrial target sites for BL- induced effects in mitochondria. Mitochondria have five complexes, I, II, III, IV and V and some of the inhibitors suppressed the increase in motility and mitochondrial membrane potential. Although the target sites have yet to be elucidated, it is suggested that the mitochondrial electron transfer chain and ATP biosynthesis are important in the suppression of age-related decline of motility.

In order to analyze in more detail the mechanism of the bioactive activity of bifidobacterium that have been identified so far, the proteins in the insulin signaling pathway and p38 Mitogen Activated Protein Kinase (MAPK) pathway, which are signaling pathways involved in aging and stress tolerance, were analyzed in measure of oxidative stress tolerance, lifespan, and motility in the deficient mutants. Consequently, the phenotypes induced by BL were suppressed. These results suggested that BL caused the above bioactive effects through these signaling pathways. In addition to the previously revealed mechanism, I have further elucidated the mechanism.

Among the bioactive effects of bifidobacterium revealed in this study, the inhibition of age-related loss of motility and effects on muscle and mitochondria in C. elegans have not been reported to date. Although future studies in mice and other higher animals will be necessary, improving motility in aging individuals and maintaining muscle and mitochondrial function could prevent sarcopenia, a decline in muscle and motility with aging, and extend health span. Bifidobacterium intake may also develop into an inhibitory effect on Parkinson's disease (PD). PD is caused by aging and other factors and reduces mitochondrial homeostasis. Consequently, this causes dopaminergic neuronal degeneration. In the present study BL maintained the mitochondrial membrane potential in aging nematodes. This suggests that mitochondrial homeostasis is maintained and that BL has the potential to prevent PD. In the future, I plan to analyze the effects of bifidobacterium on preventing sarcopenia and inhibiting PD.

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