β-Sitosterol Attenuates Dexamethasone-Induced Muscle Atrophy via Regulating FoxO1-Dependent Signaling in C2C12 Cell and Mice Model
Sarcopenia refers to a decline in muscle mass and strength with age, causing significant impairment in the ability to carry out normal daily functions and increased risk of falls and fractures, eventually leading to loss of independence. Maintaining protein homeostasis is an important factor in prev...
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MDPI AG
2022-07-01
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| Series: | Nutrients |
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| Online Access: | https://www.mdpi.com/2072-6643/14/14/2894 |
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| author | Young-Sool Hah Won Keong Lee Sangyeob Lee Eun Ji Kim Jung Hyeon Lee Seung-Jun Lee Yeong Ho Ji Sang Gon Kim Hyeong-Hwan Lee Seo Yeon Hong Jun-Il Yoo |
| author_facet | Young-Sool Hah Won Keong Lee Sangyeob Lee Eun Ji Kim Jung Hyeon Lee Seung-Jun Lee Yeong Ho Ji Sang Gon Kim Hyeong-Hwan Lee Seo Yeon Hong Jun-Il Yoo |
| author_sort | Young-Sool Hah |
| collection | DOAJ |
| description | Sarcopenia refers to a decline in muscle mass and strength with age, causing significant impairment in the ability to carry out normal daily functions and increased risk of falls and fractures, eventually leading to loss of independence. Maintaining protein homeostasis is an important factor in preventing muscle loss, and the decrease in muscle mass is caused by an imbalance between anabolism and catabolism of muscle proteins. Although β-sitosterol has various effects such as anti-inflammatory, protective effect against nonalcoholic fatty liver disease (NAFLD), antioxidant, and antidiabetic activity, the mechanism of β-sitosterol effect on the catabolic pathway was not well known. β-sitosterol was assessed in vitro and in vivo using a dexamethasone-induced muscle atrophy mice model and C2C12 myoblasts. β-sitosterol protected mice from dexamethasone-induced muscle mass loss. The thickness of gastrocnemius muscle myofibers was increased in dexamethasone with the β-sitosterol treatment group (DS). Grip strength and creatine kinase (CK) activity were also recovered when β-sitosterol was treated. The muscle loss inhibitory efficacy of β-sitosterol in dexamethasone-induced muscle atrophy in C2C12 myotube was also verified in C2C12 myoblast. β-sitosterol also recovered the width of myotubes. The protein expression of muscle atrophy F-box (MAFbx) was increased in dexamethasone-treated animal models and C2C12 myoblast, but it was reduced when β-sitosterol was treated. MuRF1 also showed similar results to MAFbx in the mRNA level of C2C12 myotubes. In addition, in the gastrocnemius and tibialis anterior muscles of mouse models, Forkhead Box O1 (FoxO1) protein was increased in the dexamethasone-treated group (Dexa) compared with the control group and reduced in the DS group. Therefore, β-sitosterol would be a potential treatment agent for aging sarcopenia. |
| first_indexed | 2024-03-09T06:05:20Z |
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| institution | Directory Open Access Journal |
| issn | 2072-6643 |
| language | English |
| last_indexed | 2024-03-09T06:05:20Z |
| publishDate | 2022-07-01 |
| publisher | MDPI AG |
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| spelling | doaj.art-5d39aedb41fd4f26aa30368982de96202023-12-03T12:04:27ZengMDPI AGNutrients2072-66432022-07-011414289410.3390/nu14142894β-Sitosterol Attenuates Dexamethasone-Induced Muscle Atrophy via Regulating FoxO1-Dependent Signaling in C2C12 Cell and Mice ModelYoung-Sool Hah0Won Keong Lee1Sangyeob Lee2Eun Ji Kim3Jung Hyeon Lee4Seung-Jun Lee5Yeong Ho Ji6Sang Gon Kim7Hyeong-Hwan Lee8Seo Yeon Hong9Jun-Il Yoo10Department of Orthopedics, Institute of Health Sciences, Gyeongsang National University School of Medicine, Jinju 52727, KoreaBiomedical Research Institute, Gyeongsang National University Hospital, Jinju 52727, KoreaBiomedical Research Institute, Gyeongsang National University Hospital, Jinju 52727, KoreaBiomedical Research Institute, Gyeongsang National University Hospital, Jinju 52727, KoreaDepartment of Orthopedics, Institute of Health Sciences, Gyeongsang National University School of Medicine, Jinju 52727, KoreaDepartment of Convergence of Medical Sciences, Gyeongsang National University, Jinju 52828, KoreaDepartment of Convergence of Medical Sciences, Gyeongsang National University, Jinju 52828, KoreaAnti-Aging Research Group, Gyeongnam Oriental Anti-Aging Institute, Sancheong 52215, KoreaAnti-Aging Research Group, Gyeongnam Oriental Anti-Aging Institute, Sancheong 52215, KoreaCrop Production Technology Research Division, NICS, RDA, Miryang 50424, KoreaDepartment of Orthopedics, Institute of Health Sciences, Gyeongsang National University School of Medicine, Jinju 52727, KoreaSarcopenia refers to a decline in muscle mass and strength with age, causing significant impairment in the ability to carry out normal daily functions and increased risk of falls and fractures, eventually leading to loss of independence. Maintaining protein homeostasis is an important factor in preventing muscle loss, and the decrease in muscle mass is caused by an imbalance between anabolism and catabolism of muscle proteins. Although β-sitosterol has various effects such as anti-inflammatory, protective effect against nonalcoholic fatty liver disease (NAFLD), antioxidant, and antidiabetic activity, the mechanism of β-sitosterol effect on the catabolic pathway was not well known. β-sitosterol was assessed in vitro and in vivo using a dexamethasone-induced muscle atrophy mice model and C2C12 myoblasts. β-sitosterol protected mice from dexamethasone-induced muscle mass loss. The thickness of gastrocnemius muscle myofibers was increased in dexamethasone with the β-sitosterol treatment group (DS). Grip strength and creatine kinase (CK) activity were also recovered when β-sitosterol was treated. The muscle loss inhibitory efficacy of β-sitosterol in dexamethasone-induced muscle atrophy in C2C12 myotube was also verified in C2C12 myoblast. β-sitosterol also recovered the width of myotubes. The protein expression of muscle atrophy F-box (MAFbx) was increased in dexamethasone-treated animal models and C2C12 myoblast, but it was reduced when β-sitosterol was treated. MuRF1 also showed similar results to MAFbx in the mRNA level of C2C12 myotubes. In addition, in the gastrocnemius and tibialis anterior muscles of mouse models, Forkhead Box O1 (FoxO1) protein was increased in the dexamethasone-treated group (Dexa) compared with the control group and reduced in the DS group. Therefore, β-sitosterol would be a potential treatment agent for aging sarcopenia.https://www.mdpi.com/2072-6643/14/14/2894β-sitosterolFoxO1dexamethasonemuscle atrophyMuRF1MAFbx |
| spellingShingle | Young-Sool Hah Won Keong Lee Sangyeob Lee Eun Ji Kim Jung Hyeon Lee Seung-Jun Lee Yeong Ho Ji Sang Gon Kim Hyeong-Hwan Lee Seo Yeon Hong Jun-Il Yoo β-Sitosterol Attenuates Dexamethasone-Induced Muscle Atrophy via Regulating FoxO1-Dependent Signaling in C2C12 Cell and Mice Model Nutrients β-sitosterol FoxO1 dexamethasone muscle atrophy MuRF1 MAFbx |
| title | β-Sitosterol Attenuates Dexamethasone-Induced Muscle Atrophy via Regulating FoxO1-Dependent Signaling in C2C12 Cell and Mice Model |
| title_full | β-Sitosterol Attenuates Dexamethasone-Induced Muscle Atrophy via Regulating FoxO1-Dependent Signaling in C2C12 Cell and Mice Model |
| title_fullStr | β-Sitosterol Attenuates Dexamethasone-Induced Muscle Atrophy via Regulating FoxO1-Dependent Signaling in C2C12 Cell and Mice Model |
| title_full_unstemmed | β-Sitosterol Attenuates Dexamethasone-Induced Muscle Atrophy via Regulating FoxO1-Dependent Signaling in C2C12 Cell and Mice Model |
| title_short | β-Sitosterol Attenuates Dexamethasone-Induced Muscle Atrophy via Regulating FoxO1-Dependent Signaling in C2C12 Cell and Mice Model |
| title_sort | β sitosterol attenuates dexamethasone induced muscle atrophy via regulating foxo1 dependent signaling in c2c12 cell and mice model |
| topic | β-sitosterol FoxO1 dexamethasone muscle atrophy MuRF1 MAFbx |
| url | https://www.mdpi.com/2072-6643/14/14/2894 |
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