Celastrol and Rhynchophylline in the mitigation of simulated muscle atrophy under in vitro.
Saudi Pharm J
; 30(10): 1387-1395, 2022 Oct.
Article
em En
| MEDLINE
| ID: mdl-36387339
ABSTRACT
Muscular atrophy (MA) is a disease of various origins, i.e., genetic or the most common, caused by mechanical injury. So far, there is no universal therapeutic model because this disease is often progressive with numerous manifested symptoms. Moreover, there is no safe and low-risk therapy dedicated to muscle atrophy. For this reason, our research focuses on finding an alternative method using natural compounds to treat MA. This study proposes implementing natural substances such as celastrol and Rhynchophylline on the cellular level, using a simulated and controlled atrophy process. Methods:
Celastrol and Rhynchophylline were used as natural compounds against simulated atrophy in C2C12 cells. Skeletal muscle C2C12 cells were stimulated for the differentiation process. Atrophic conditions were obtained by the exposure to the low concertation of doxorubicin and validated by FoxO3 and MAFbx. The protective and regenerative effect of drugs on cell proliferation was determined by the MTT assay and MT-CO1, VDAC1, and prohibitin expression.Results:
The obtained results revealed that both natural substances reduced atrophic symptoms. Rhynchophylline and celastrol attenuated atrophic cells in the viability studies, morphology analysis by diameter measurements, modulated prohibitin VDAC, and MT-CO1 expression.Conclusions:
The obtained results revealed that celastrol and Rhynchophylline could be effectively used as a supportive treatment in atrophy-related disorders. Thus, natural drugs seem promising for muscle regeneration.
Akt1, serine/threonine-protein kinase or AKT kinase 1; CLS, celastrol; Celastrol; DEX, dexamethasone; DOX, doxorubicin; ERK1/2, extracellular signal-regulated kinase 1/2; HSF1, Heat shock factor 1; HSP, heat shock protein; ICC, immunocytochemistry; MA, Muscular atrophy; MAFbx, Muscle Atrophy F-box gene; MMP, mitochondrial membrane potential; MTCO1, Mitochondrially Encoded Cytochrome C Oxidase I; MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; MuRF1, Muscle RING Finger protein-1; Muscle atrophy; NLS, nuclear localization signals; RA, rheumatoid arthritis; Rhynchophylline; Ryn, Rhynchophylline; SMA, spinal muscular atrophy; Skeletal muscles; VDAC, voltage-dependent anion channel; mPTP, mitochondrial permeability transition pore
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Base de dados:
MEDLINE
Tipo de estudo:
Prognostic_studies
Idioma:
En
Ano de publicação:
2022
Tipo de documento:
Article