scholarly journals Fermented ginseng leaf enriched with rare ginsenosides relieves exercise-induced fatigue via regulating metabolites of muscular interstitial fluid, satellite cells-mediated muscle repair and gut microbiota

2021 ◽  
Vol 83 ◽  
pp. 104509
Author(s):  
Ziyi Zheng ◽  
Guo Xie ◽  
Hongxia Liu ◽  
Guiliang Tan ◽  
Lin Li ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Satellite Cells ◽  
Interstitial Fluid ◽  
Muscle Repair ◽  
Fermented Ginseng ◽  
Exercise Induced ◽  
Ginseng Leaf

scholarly journals Stimulating effect of fermented ginseng leaf saponin on the differentiation and mineralization of murine osteoblastic MC3T3-E1 cells

2019 ◽  
Vol 54 (2) ◽  
pp. 147-154
Author(s):  
MA Huq ◽  
MH Siddiqi ◽  
YJ Kim ◽  
S Akter ◽  
DC Yang
Keyword(s):  
Good Effect ◽  
Dependent Manner ◽  
Osteoporosis Prevention ◽  
Ginsenoside Rd ◽  
Fermented Product ◽  
Fermented Ginseng ◽  
Pharmacologically Active ◽  
Short Time ◽  
Dose Dependent ◽  
Ginseng Leaf

In this study, abundant ginseng leaf saponins were converted into minor ginsenosides that havemore pharmacological efficacy via fermentation process using recombinant β-glucosidase (bgp1). This fermented product was used to investigate the stimulatory effect on differentiation and mineralization of murine osteoblastic MC3T3-E1 cells. All major ginsenosides which areavailable in ginseng leaf were biotransformed into more pharmacologically active minor ginsenosides within a short time of incubation. The results showed that 100% of ginsenoside Rd, Rg1and Re were decomposed and transformed to Rg3, Rh1and Rg2, respectively within 03 (three) hours of incubation. Ginseng leaf saponin contains 17.1% Rg1, 44.9% Re, 10.8% Rd, 4.8% Rb1, 5.7% Rb2, 6.9% Rc,2.7% Rg2, and 6.8% F1 ginsenoside. But after fermentation, the products contain mostly pharmacological active minor ginsenosides including 42.2% Rg2, 13.7% Rg3, 8.8% Rh1, 4.9% F1 and 3.6% PPT ginsenosides. Moreover, we investigated and compared the effect of leaf saponins (LS) and fermented leaf saponins (FLS), on the differentiation and mineralization of pre-osteoblastic MC3T3-E1 cells. Treatment with FLS remarkably enhanced cell viability in a dose-dependent manner. FLS notably stimulated the ALP activity, Coll-I synthesis and mineralization ability of MC3T3-E1 cells. Based on the comparison between LS and FLS, it is clear that FLS has good effect on differentiation of osteoblastic MC3T3-E1 cells and bone formation. Therefore, bgp1-fermented ginseng leaf saponins could be a novel treatment for osteoporosis prevention. Bangladesh J. Sci. Ind. Res.54(2), 147-154, 2019

Effects of fermented ginseng on the gut microbiota and immunity of rats with antibiotic-associated diarrhea

2021 ◽  
Vol 267 ◽  
pp. 113594
Author(s):  
Qingsong Qu ◽  
Fang Yang ◽  
Chongyan Zhao ◽  
Xing Liu ◽  
Pengshuo Yang ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Antibiotic Associated Diarrhea ◽  
Fermented Ginseng

scholarly journals Stem cells for skeletal muscle repair

2011 ◽  
Vol 366 (1575) ◽  
pp. 2297-2306 ◽  
Author(s):  
Jennifer L. Shadrach ◽  
Amy J. Wagers
Keyword(s):  
Skeletal Muscle ◽  
Stem Cells ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Cell Function ◽  
Therapeutic Potential ◽  
Muscle Disease ◽  
Muscle Fibres ◽  
Muscle Repair ◽  
Muscle Satellite Cells

Skeletal muscle is a highly specialized tissue composed of non-dividing, multi-nucleated muscle fibres that contract to generate force in a controlled and directed manner. Skeletal muscle is formed during embryogenesis from a subset of muscle precursor cells, which generate both differentiated muscle fibres and specialized muscle-forming stem cells known as satellite cells. Satellite cells remain associated with muscle fibres after birth and are responsible for muscle growth and repair throughout life. Failure in satellite cell function can lead to delayed, impaired or failed recovery after muscle injury, and such failures become increasingly prominent in cases of progressive muscle disease and in old age. Recent progress in the isolation of muscle satellite cells and elucidation of the cellular and molecular mediators controlling their activity indicate that these cells represent promising therapeutic targets. Such satellite cell-based therapies may involve either direct cell replacement or development of drugs that enhance endogenous muscle repair mechanisms. Here, we discuss recent breakthroughs in understanding both the cell intrinsic and extrinsic regulators that determine the formation and function of muscle satellite cells, as well as promising paths forward to realizing their full therapeutic potential.

scholarly journals PGC-1α in the myofibers regulates the balance between myogenic and adipogenic progenitors affecting muscle regeneration

2021 ◽  
Author(s):  
Marc Beltrà ◽  
Fabrizio Pin ◽  
Domiziana Costamagna ◽  
Robin Duelen ◽  
Alessandra Renzini ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cells ◽  
Stromal Cells ◽  
Muscle Regeneration ◽  
Peroxisome Proliferator ◽  
Muscle Repair ◽  
Metabolic State ◽  
Peroxisome Proliferator Activated Receptor ◽  
The Relationship

Skeletal muscle repair is accomplished by satellite cells (MuSC) in cooperation with interstitial stromal cells (ISCs). So far, the relationship between the function of these cells and the metabolic state of myofibers remains unclear. The present study reports alterations in the proportion of both MuSCs and adipogenesis regulators (Aregs) induced by overexpression of peroxisome proliferator-activated receptor gamma coactivator 1–alpha (PGC–1α) in the myofibers (MCK–PGC–1α mice). Although PGC-1α–driven increase of MuSCs does not accelerate muscle regeneration, myogenic progenitors isolated from MCK–PGC–1α mice and transplanted into intact and regenerating muscles are more prone to fuse with recipient myofibers than those derived from WT donors. Moreover, both young and aged MCK-PGC-1α animals show reduced perilipin-positive areas when challenged with an adipogenic stimulus, demonstrating low propensity to accumulate adipocytes within the muscle. These results provide new insights on the role played by PGC–1α in promoting myogenesis and hindering adipogenesis in the skeletal muscle.

scholarly journals Androgen receptor regulates the proliferation of myoblasts under appropriate or excessive stretch through IGF-1 receptor mediated p38 and ERK1/2 pathways

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Shaoting Fu ◽  
Xiaojing Lin ◽  
Lijun Yin ◽  
Xiaohui Wang
Keyword(s):  
Androgen Receptor ◽  
Muscle Mass ◽  
Satellite Cells ◽  
C2c12 Cells ◽  
C2c12 Myoblasts ◽  
Excessive Exercise ◽  
L6 Cells ◽  
Proliferation And Differentiation ◽  
Exercise Induced ◽  
P38 Pathway

Abstract Background Androgen receptor (AR) exerts important roles in exercise-induced alterations of muscle mass, in which the proliferation and differentiation of satellite cells or myoblasts are crucial. Our previous study in C2C12 myoblasts demonstrated that 15% (mimic appropriate exercise) and 20% (mimic excessive exercise) stretches promoted and inhibited the proliferation respectively; and AR played a crucial role in 15% stretch-induced pro-proliferation through IGF-1-modulated PI3K/Akt, p38 and ERK1/2 pathways, but AR’s role in stretches-modulated proliferation of general myoblasts, especially 20% stretch, remains unclear, and the mechanisms need to be further clarified. Methods Firstly, the discrepancy in proliferation and the above indicators between L6 (without AR) and C2C12 (with AR) myoblasts were compared under 15% or 20% stretch. Then the influences of transfection AR or exogenous IGF-1 treatment on proliferation and these indicators were detected in stretched L6 myoblasts. Results (1) Under un-stretched state, the proliferation of L6 was slower than C2C12 cells. Furthermore, AR knockdown in C2C12 myoblasts repressed, while AR overexpression in L6 myoblasts promoted the proliferation. (2) 15% stretch-induced increases in the proliferation and activities of p38 and ERK1/2 were lower in L6 than C2C12 cells; AR overexpression enhanced the proliferation of 15% stretched L6 cells accompanied with the increases of p38 and ERK1/2 activities. (3) 20% stretch-induced anti-proliferation and inhibition of p38 activity were severer in L6 than C2C12 myoblasts; AR overexpression reversed the anti-proliferation of 20% stretch and enhanced p38 activity in L6 myoblasts. (4) In stretched L6 myoblasts, AR overexpression increased IGF-1R level despite no detectable IGF-1; and recombinant IGF-1 increased the proliferation, the level of IGF-1R, and the activities of p38 and ERK1/2 in 15% stretched L6 myoblasts. Conclusions The study demonstrated AR's crucial roles in stretches-regulated proliferation of myoblasts, and increased AR fulfilled 15% stretch's pro-proliferation via activating IGF-1R- p38 and ERK1/2 pathways while decreased AR achieved 20% stretch's anti-proliferation via inhibiting IGF-1R- p38 pathway, which is useful to understand in depth the role and mechanisms of AR in appropriate exercise increasing while excessive exercise decreasing muscle mass.

scholarly journals Rejuvenating stem cells to restore muscle regeneration in aging

F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 76 ◽  
Author(s):  
Eyal Bengal ◽  
Eusebio Perdiguero ◽  
Antonio L. Serrano ◽  
Pura Muñoz-Cánoves
Keyword(s):  
Stem Cells ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Environmental Changes ◽  
Local Environment ◽  
The Elderly ◽  
Muscle Repair ◽  
Extrinsic Factors ◽  
Repair Capacity ◽  
Cell Dysfunction

Adult muscle stem cells, originally called satellite cells, are essential for muscle repair and regeneration throughout life. Besides a gradual loss of mass and function, muscle aging is characterized by a decline in the repair capacity, which blunts muscle recovery after injury in elderly individuals. A major effort has been dedicated in recent years to deciphering the causes of satellite cell dysfunction in aging animals, with the ultimate goal of rejuvenating old satellite cells and improving muscle function in elderly people. This review focuses on the recently identified network of cell-intrinsic and -extrinsic factors and processes contributing to the decline of satellite cells in old animals. Some studies suggest that aging-related satellite-cell decay is mostly caused by age-associated extrinsic environmental changes that could be reversed by a “youthful environment”. Others propose a central role for cell-intrinsic mechanisms, some of which are not reversed by environmental changes. We believe that these proposals, far from being antagonistic, are complementary and that both extrinsic and intrinsic factors contribute to muscle stem cell dysfunction during aging-related regenerative decline. The low regenerative potential of old satellite cells may reflect the accumulation of deleterious changes during the life of the cell; some of these changes may be inherent (intrinsic) while others result from the systemic and local environment (extrinsic). The present challenge is to rejuvenate aged satellite cells that have undergone reversible changes to provide a possible approach to improving muscle repair in the elderly.

Sign in / Sign up

Export Citation Format

Share Document