The Extract of
3T3-L1 Cells
AMP-Activated Protein Kinases
/ metabolism
Adipose Tissue
/ pathology
Animals
Arctium
/ chemistry
Atrophy
/ prevention & control
Cachexia
/ drug therapy
Gene Expression
/ drug effects
Interleukin-6
/ genetics
Male
Mice
Mice, Inbred BALB C
Muscle, Skeletal
/ pathology
Neoplasms
/ complications
Phytotherapy
Plant Extracts
/ isolation & purification
Tumor Cells, Cultured
Uncoupling Protein 1
/ genetics
Weight Loss
/ drug effects
3T3-L1 cells
Arctii Fructus
C2C12 myoblast
browning
cancer cachexia
Journal
Nutrients
ISSN: 2072-6643
Titre abrégé: Nutrients
Pays: Switzerland
ID NLM: 101521595
Informations de publication
Date de publication:
19 Oct 2020
19 Oct 2020
Historique:
received:
01
09
2020
revised:
13
10
2020
accepted:
14
10
2020
entrez:
22
10
2020
pubmed:
23
10
2020
medline:
21
4
2021
Statut:
epublish
Résumé
Cachexia induced by cancer is a systemic wasting syndrome and it accompanies continuous body weight loss with the exhaustion of skeletal muscle and adipose tissue. Cancer cachexia is not only a problem in itself, but it also reduces the effectiveness of treatments and deteriorates quality of life. However, effective treatments have not been found yet. Although Arctii Fructus (AF) has been studied about several pharmacological effects, there were no reports on its use in cancer cachexia. To induce cancer cachexia in mice, we inoculated CT-26 cells to BALB/c mice through subcutaneous injection and intraperitoneal injection. To mimic cancer cachexia in vitro, we used conditioned media (CM), which was CT-26 colon cancer cells cultured medium. In in vivo experiments, AF suppressed expression of interleukin (IL)-6 and atrophy of skeletal muscle and adipose tissue. As a result, the administration of AF decreased mortality by preventing weight loss. In adipose tissue, AF decreased expression of uncoupling protein 1 (UCP1) by restoring AMP-activated protein kinase (AMPK) activation. In in vitro model, CM increased muscle degradation factors and decreased adipocytes differentiation factors. However, these tendencies were ameliorated by AF treatment in C2C12 myoblasts and 3T3-L1 cells. Taken together, our study demonstrated that AF could be a therapeutic supplement for patients suffering from cancer cachexia.
Sections du résumé
BACKGROUND
BACKGROUND
Cachexia induced by cancer is a systemic wasting syndrome and it accompanies continuous body weight loss with the exhaustion of skeletal muscle and adipose tissue. Cancer cachexia is not only a problem in itself, but it also reduces the effectiveness of treatments and deteriorates quality of life. However, effective treatments have not been found yet. Although Arctii Fructus (AF) has been studied about several pharmacological effects, there were no reports on its use in cancer cachexia.
METHODS
METHODS
To induce cancer cachexia in mice, we inoculated CT-26 cells to BALB/c mice through subcutaneous injection and intraperitoneal injection. To mimic cancer cachexia in vitro, we used conditioned media (CM), which was CT-26 colon cancer cells cultured medium.
RESULTS
RESULTS
In in vivo experiments, AF suppressed expression of interleukin (IL)-6 and atrophy of skeletal muscle and adipose tissue. As a result, the administration of AF decreased mortality by preventing weight loss. In adipose tissue, AF decreased expression of uncoupling protein 1 (UCP1) by restoring AMP-activated protein kinase (AMPK) activation. In in vitro model, CM increased muscle degradation factors and decreased adipocytes differentiation factors. However, these tendencies were ameliorated by AF treatment in C2C12 myoblasts and 3T3-L1 cells.
CONCLUSION
CONCLUSIONS
Taken together, our study demonstrated that AF could be a therapeutic supplement for patients suffering from cancer cachexia.
Identifiants
pubmed: 33086629
pii: nu12103195
doi: 10.3390/nu12103195
pmc: PMC7603378
pii:
doi:
Substances chimiques
Interleukin-6
0
Plant Extracts
0
Uncoupling Protein 1
0
AMP-Activated Protein Kinases
EC 2.7.11.31
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : National Research Foundation of Korea
ID : 2018R1C1B6002722
Organisme : National Research Foundation of Korea
ID : 2018R1D1A3B07040871
Organisme : National Research Foundation of Korea
ID : 2019R1I1A3A01060998
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
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