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KR-102961976-B1 - novel Lactic Acid Bacteria and Composition comprising the same for myoblast proliferation myotube differentiation, and muscle atrophy inhibition

KR102961976B1KR 102961976 B1KR102961976 B1KR 102961976B1KR-102961976-B1

Abstract

The present invention provides the Fructobacillus fructosus ACG3-100 strain deposited under accession number KCTC16556BP and its derivatives, which have effective effects in preventing and treating diseases related to muscle weakness or muscle atrophy and improving muscle strength by promoting the proliferation of myoblasts and differentiation of myotubes and inhibiting muscle atrophy.

Inventors

  • 권순재
  • 김혜리
  • 최우진
  • 이승헌
  • 최보빈
  • 이반석

Assignees

  • 주식회사 어큐진

Dates

Publication Date
20260508
Application Date
20251128

Claims (8)

  1. Fructobacillus fructosus ACG3-100 strain deposited under accession number KCTC16556BP.
  2. A derivative of the Fructobacillus fructosus ACG3-100 strain deposited under accession number KCTC16556BP, characterized by being any one of the culture of the Fructobacillus fructosus ACG3-100 strain deposited under accession number KCTC16556BP, the lysate of the strain, or the culture supernatant of the strain.
  3. A pharmaceutical composition for the prevention and treatment of sarcopenia, muscular atrophy, or muscle weakness, characterized by comprising, as an oily component, one or more selected from the Fructobacillus fructosus ACG3-100 strain deposited under accession number KCTC16556BP, its culture, its lysate, or its culture supernatant.
  4. In paragraph 3, The above pharmaceutical composition is characterized by inhibiting the production of nitric oxide (NO) to suppress an inflammatory response.
  5. A food composition for the prevention and improvement of sarcopenia, muscular atrophy, or muscle weakness, characterized by comprising, as an oily component, one or more selected from the Fructobacillus fructosus ACG3-100 strain deposited under accession number KCTC16556BP, its culture, its lysate, or its culture supernatant.
  6. In paragraph 5, The above food composition is characterized by inhibiting the production of nitric oxide (NO) to suppress an inflammatory response.
  7. delete
  8. delete

Description

Novel Lactic Acid Bacteria and Composition comprising the same for myoblast proliferation, myotube differentiation, and muscle atrophy inhibition The present invention relates to a novel lactic acid bacterium and a composition containing the same, which has effective effects in preventing and treating diseases related to muscle weakness or muscle atrophy and improving muscle strength by promoting the proliferation of myoblasts and myotube differentiation and inhibiting muscle atrophy. Muscles are tissues that play a pivotal role in the human body's movement, posture maintenance, and metabolic regulation, making them a critical physiological element directly linked to a healthy life. When muscle mass and function decline due to aging, disease, or lack of exercise, conditions such as sarcopenia and muscular atrophy are induced. Sarcopenia and atrophy are commonly observed not only in the elderly but also in individuals with chronic diseases, obesity, and sedentary lifestyles; the resulting decrease in muscle strength and reduced motor function lead to a decline in quality of life and various secondary complications. Therefore, promoting muscle proliferation and differentiation, as well as inhibiting muscular atrophy, are emerging as important research areas for health improvement, disease prevention, and treatment. Meanwhile, the Akt (Protein kinase B) signaling pathway plays a central role in the muscle growth process. Akt activates mTOR (mammalian target of rapamycin) to promote protein synthesis and cell growth, while simultaneously inhibiting the activity of the FoxO3a (Forhead box 3a) transcription factor, thereby reducing the expression of genes associated with muscle atrophy (such as MuRF1 and Atrogin-1). Through this pathway, muscle loss can be suppressed, and muscle growth and differentiation can be promoted. Furthermore, Akt signaling is involved in maintaining intracellular energy metabolism and mitochondrial function, optimizing the environment for muscle cell survival and regeneration. Conversely, a decrease in Akt activity or inhibition of mTOR signaling leads to reduced protein synthesis and increased expression of FOXO3a-mediated muscle atrophy genes, inducing sarcopenia. Therefore, the Akt-mTOR-FOXO3a axis serves as a key molecular pathway regulating muscle homeostasis and acts as a crucial regulatory axis determining the balance between muscle growth and atrophy. Furthermore, nitric oxide (NO) plays a crucial role in muscle regeneration and inflammation regulation by increasing intramuscular blood flow, activating satellite cells, and inducing anti-inflammatory effects. Excessive NO production induces oxidative stress within muscle cells and impairs energy metabolism by degrading mitochondrial function. This leads to reduced protein synthesis and the activation of the ubiquitin-proteasome pathway, which promotes muscle protein degradation. Moreover, high levels of NO stimulate the FOXO-3α pathway, increasing the expression of genes associated with muscle atrophy (such as MuRF1 and Atrogin-1) and accelerating muscle fiber loss over the long term. Therefore, while NO production serves a physiological role at certain levels, it acts as a major factor inducing muscle loss when excessive. Recently, various biological compositions and therapeutic agents for promoting muscle health have been developed; however, the demand for effective and safe compositions for muscle proliferation and maintenance of function remains high. In particular, compositions containing lactic acid bacteria and their metabolites are attracting attention as a novel approach to promoting muscle cell proliferation and differentiation while inhibiting muscle atrophy, making it necessary to develop compositions for improving muscle health utilizing these agents. Figure 1 shows the results of comparing the degree of myoblast proliferation promotion in C2C12 cells following treatment with F. fructosus ACG3-100. Figures 2a and 2b show the results of confirming the protein expression patterns involved in muscle synthesis in C2C12 cells following treatment with F. fructosus ACG3-100 during the muscle cell proliferation stage. Figures 3a and 3b show the results of comparing the degree of myotube differentiation promotion in C2C12 cells following treatment with F. fructosus ACG3-100. Figures 4a and 4b show the results of confirming the protein expression patterns involved in muscle synthesis in C2C12 cells following treatment with F. fructosus ACG3-100 at the myotube differentiation stage. Figures 5a and 5b show the results of comparing the degree of muscle atrophy in C2C12 cells following treatment with F. fructosus ACG3-100. Figures 6a, b, and c show the expression patterns of proteins involved in muscle synthesis and proteins involved in muscle atrophy in C2C12 cells following treatment with F. fructosus ACG3-100 at the muscle atrophy stage. Figure 7 shows the inhibitory effect of F. fructosus ACG3-100 on NO production in LPS-stimul