KR-20240113660-A9 - Lactobacillus rhamnosus JY02 and composition for preventing, improving or treating muscle diseases comprising the same

Abstract

The present invention relates to a novel strain of Lactobacillus rhamnosus JY02 and a composition for preventing, improving, or treating muscle diseases containing the same. The Lactobacillus rhamnosus JY02 strain according to the present invention inhibits the expression of MuRF1 and atrogin-1, which are representative factors involved in the degradation of muscle proteins, and has the effect of inducing the expression of the gene MyoD, which is related to muscle synthesis and differentiation. Therefore, it can be usefully used in fields such as pharmaceuticals, food, feed, feed additives, drinking water, compositions for promoting muscle differentiation, muscle regeneration, or muscle strengthening, which can prevent, improve, or treat muscle diseases including sarcopenia and muscular atrophy.

Inventors

• 오상남
• 강민경
• 이주연
• 유지선
• 이수정

Assignees

• 전주대학교 산학협력단

Dates

Publication Date

20260513

Application Date

20230113

Claims (13)

1. Lactobacillus rhamnosus JY02 strain.
2. In paragraph 1, The strain is characterized by comprising the 16S rRNA sequence of SEQ ID NO. 1.
3. In paragraph 1, The strain described above is characterized by being deposited under accession number KACC81207BP.
4. A pharmaceutical composition for the prevention or treatment of muscle diseases comprising the strain of Lactobacillus rhamnosus JY02 deposited under accession number KACC81207BP or cells thereof as an active ingredient.
5. In paragraph 4, A pharmaceutical composition for the prevention or treatment of muscle disease, characterized in that the above-mentioned muscle disease is sarcopenia.
6. In paragraph 5, A pharmaceutical composition for the prevention or treatment of muscle diseases, characterized in that the sarcopenia is selected from the group consisting of muscular atrophy, disuse atrophy, spinal muscular amyotrophy, dystrophy, rigidity, muscular hypotonia, muscle weakness, muscular dystrophy, amyotrophic lateral sclerosis, sphinobulbar muscular atrophy, and myasthenia gravis.
7. In paragraph 1, A pharmaceutical composition for the prevention or treatment of muscle diseases, characterized by further comprising a pharmaceutically acceptable carrier, excipient, or diluent.
8. A food for the prevention or improvement of muscle diseases comprising the strain of Lactobacillus rhamnosus JY02 deposited under accession number KACC81207BP or cells thereof as an active ingredient.
9. In paragraph 8, A food for the prevention or improvement of muscle diseases, characterized by additionally containing a food-grade acceptable dietary additive.
10. A feed additive for the prevention or improvement of muscle diseases comprising the strain of Lactobacillus rhamnosus JY02 deposited under accession number KACC81207BP or cells thereof as an active ingredient.
11. A feed composition for the prevention or improvement of muscle diseases comprising the strain of Lactobacillus rhamnosus JY02 deposited under accession number KACC81207BP or cells thereof as an active ingredient.
12. A drinking water additive for the prevention or improvement of muscle diseases comprising the strain of Lactobacillus rhamnosus JY02 deposited under accession number KACC81207BP or cells thereof as an active ingredient.
13. A composition for promoting muscle differentiation, muscle regeneration, or muscle strengthening comprising the Lactobacillus rhamnosus JY02 strain deposited under accession number KACC81207BP or cells thereof as an active ingredient.

Description

Lactobacillus rhamnosus JY02 strain and composition for preventing, improving or treating muscle diseases comprising the same The present invention relates to a novel strain of Lactobacillus rhamnosus JY02 and a composition for preventing, improving, or treating muscle diseases containing the same. Muscle diseases cause impairment in walking and mobility due to the weakening of skeletal muscles, making activities of daily living (ADL) difficult, leading to cardiopulmonary dysfunction, and can cause other complications. Diseases that cause muscle weakness include sarcopenia, which progresses with aging; muscle atrophy, caused by imbalances in protein metabolism or reduced muscle use; starvation; wasting diseases (such as cancer); and acardiotrophy, which also progresses with aging. Sarcopenia is known to involve not only a decline in muscle strength due to a decrease in muscle mass, but also the degeneration of motor neurons that induce skeletal muscle contraction, which prevents contraction; or the reduced or altered expression of proteins involved in muscle contraction within the skeletal muscle, which prevents normal contraction; and in the long term, the aforementioned motor neurons or skeletal muscles transform into fibrous tissue. Causes of sarcopenia include the aging of muscle-producing astrocytes, degenerative central nervous system diseases, weakened motor function, decreased activity at the neuromuscular junction, changes in endocrine hormones, increased proinflammatory cytokines, decreased mitochondrial function, and reduced physical activity. Furthermore, sarcopenia contributes to a higher prevalence of metabolic diseases such as hypertension, diabetes, arthritis, obesity, and cancer due to reduced metabolism and weakened immunity. In addition, sarcopenia is characterized not only by a decrease in muscle mass but also by changes in the types of muscle fibers. While the decline in muscle fibers due to aging involves a similar proportion of Type 1 (large, slow-contracting muscle fibers) and Type 2 (fast-contracting muscle fibers), sarcopenia is known to involve a noticeable decrease in the thickness of Type 1 muscle fibers. Meanwhile, as sarcopenia is emerging as a global public health issue, significant efforts are being made to prevent and treat it for a healthy old age. However, to date, no drugs approved by the Food and Drug Administration (FDA) to treat sarcopenia have been reported. Furthermore, while exercise and dietary therapy are non-pharmacological treatments for sarcopenia, the results vary depending on the study. Muscular atrophy refers to the weakening and degeneration of muscles caused by a progressive decrease in muscle mass. It is accelerated by inactivity, oxidative stress, and chronic inflammation, and impairs muscle function and exercise capacity. The most important factor determining muscle function is muscle mass, which is maintained by the balance between protein synthesis and breakdown. Muscular atrophy occurs when protein breakdown occurs more frequently than synthesis. Muscle size is regulated by intracellular signaling pathways that induce anabolism or catabolism within the muscle; when signaling responses inducing synthesis occur more frequently than those inducing breakdown, muscle protein synthesis increases, which manifests as an increase in muscle size or the number of muscle fibers due to the increase in muscle protein. Representative factors involved in the degradation of muscle protein include muscle-specific E3 ubiquitin ligase factors, such as atrogin-1 and MuRF-1 (Muscle RING-finger protein-1). The expression of atrogin-1 and MuRF-1 increases significantly when activity levels decrease (Foletta VC et al, Pflugers Archiv-European Journal of Physiology, 461(3), 325-335, 2011), which promotes proteosome-dependent proteolysis and leads to a decrease in muscle mass. Therefore, inhibiting the expression of atrogin-1 and MuRF-1 increases muscle protein levels, thereby increasing muscle mass. Currently, methods such as increasing mitochondrial production, muscle protein degradation inhibitors, and anti-inflammatory drugs have been proposed for the treatment of muscle atrophy, but there is currently no clear therapeutic agent available. Meanwhile, muscle cells differentiate through various muscle regulatory factors. The induction of myogenin gene expression by the expression of MyoD, a gene related to muscle synthesis and differentiation, is the most important factor in the differentiation or fusion of myoocytes and the formation of muscle tubes. Myosin heavy chain (MHC), a mediator of terminal differentiation, induces the production of muscle filaments, and the resulting bundles of muscle fibers form muscle. Furthermore, gut microbiota dysbiosis and abnormalities, which commonly occur in elderly individuals with sarcopenia, are known to directly affect muscle phenotypes. Postbiotics—byproducts such as SCFAs generated from fiber-rich diets or the consumption of probiot