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肉豆蔻提取物通过IGF1-AKT-mTOR途径和抑制自噬部分增加衰老大鼠的骨骼肌质量。

Nutmeg Extract Increases Skeletal Muscle Mass in Aging Rats Partly via IGF1-AKT-mTOR Pathway and Inhibition of Autophagy.

作者信息

Pratiwi Yuni Susanti, Lesmana Ronny, Goenawan Hanna, Sylviana Nova, Setiawan Iwan, Tarawan Vita Murniati, Lestari Keri, Abdulah Rizky, Dwipa Lazuardhi, Purba Ambrosius, Supratman Unang

机构信息

Physiology Division, Department of Biomedical Sciences, Faculty of Medicine, Universitas Padjadjaran, Jatinangor 45363, Indonesia.

Physiology Molecular Laboratory, Biological Activity Division, Central Laboratory, Universitas Padjadjaran, Jatinangor 45363, Indonesia.

出版信息

Evid Based Complement Alternat Med. 2018 Dec 17;2018:2810840. doi: 10.1155/2018/2810840. eCollection 2018.

DOI:10.1155/2018/2810840
PMID:30647761
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6311876/
Abstract

The sarcopenic phenotype is characterized by a reduction of muscle mass, a shift in fiber-type distribution, and reduced satellite cell regeneration. Sarcopenia is still a major challenge to healthy aging. Traditional Indonesian societies in Sulawesi island have been using nutmeg for maintaining health condition during aging. Interestingly, nutmeg has been known to stimulate peroxisome proliferator activated receptors (PPAR) which may contribute to myogenesis process in cardiac muscle. There is limited information about the role of nutmeg extract into physiological health benefit during aging especially myogenesis process in skeletal muscle. In the present study, we want to explore the potential effect of nutmeg in preserving skeletal muscle mass of aging rats. Aging rats, 80 weeks old, were divided into two groups (control and nutmeg). Nutmeg extract was administered for 12 weeks by gavaging. After treatment, rats were anaesthesized, then soleus and gastrocnemius muscles were collected, weighted, frozen using liquid nitrogen, and stored at -80°C until use. We observed phenomenon that nutmeg increased a little but significant food consumption on week 12, but significant decrease in body weight on weeks 10 and 12 unexpectedly increased significantly in soleus muscle weight (). Nutmeg extract increased significantly gene expression of myogenic differentiation (MyoD), paired box 7 (Pax7), myogenin, myosin heavy chain I (MHC I), and insulin-like growth factor I () in soleus muscle. Furthermore, nutmeg increased serine/threonine kinase (AKT) protein levels and activation of mammalian target of rapamycin (mTOR), inhibited autophagy activity, and stimulated or at least preserved muscle mass during aging. Taken together, nutmeg extract may increase muscle mass or prevent decrease of muscle wasting in soleus muscle by partly stimulating myogenesis, regeneration process, and preserving muscle mass via IGF-AKT-mTOR pathway leading to inhibition of autophagy activity during aging. This finding may reveal the potential nutmeg benefits as alternative supplement for preserving skeletal muscle mass and preventing sarcopenia in elderly.

摘要

肌肉减少症的表型特征为肌肉质量减少、纤维类型分布改变以及卫星细胞再生能力下降。肌肉减少症仍是健康衰老面临的一项重大挑战。苏拉威西岛的传统印度尼西亚社会一直使用肉豆蔻来维持衰老过程中的健康状况。有趣的是,已知肉豆蔻可刺激过氧化物酶体增殖物激活受体(PPAR),这可能有助于心肌的肌生成过程。关于肉豆蔻提取物在衰老过程中对生理健康益处的作用,尤其是对骨骼肌肌生成过程的作用,相关信息有限。在本研究中,我们想要探究肉豆蔻对衰老大鼠骨骼肌质量的潜在影响。80周龄的衰老大鼠被分为两组(对照组和肉豆蔻组)。通过灌胃给予肉豆蔻提取物12周。治疗后,将大鼠麻醉,然后收集比目鱼肌和腓肠肌,称重,用液氮冷冻,并储存在-80°C直至使用。我们观察到,在第12周时肉豆蔻使食物消耗量略有但显著增加,但在第10周和第12周体重显著下降,而比目鱼肌重量却意外地显著增加。肉豆蔻提取物显著增加了比目鱼肌中肌源性分化(MyoD)、配对盒7(Pax7)、肌细胞生成素、肌球蛋白重链I(MHC I)和胰岛素样生长因子I()的基因表达。此外,肉豆蔻增加了丝氨酸/苏氨酸激酶(AKT)蛋白水平和雷帕霉素哺乳动物靶标(mTOR)的激活,抑制了自噬活性,并在衰老过程中刺激或至少维持了肌肉质量。综上所述,肉豆蔻提取物可能通过部分刺激肌生成、再生过程,并通过IGF-AKT-mTOR途径维持肌肉质量,从而抑制衰老过程中的自噬活性,增加比目鱼肌的肌肉质量或防止肌肉萎缩。这一发现可能揭示了肉豆蔻作为一种替代补充剂在维持老年人骨骼肌质量和预防肌肉减少症方面的潜在益处。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e35/6311876/6c1a5c07eab9/ECAM2018-2810840.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e35/6311876/46c02da409aa/ECAM2018-2810840.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e35/6311876/df064848d354/ECAM2018-2810840.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e35/6311876/fb93b693b032/ECAM2018-2810840.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e35/6311876/519562ce50fe/ECAM2018-2810840.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e35/6311876/6c1a5c07eab9/ECAM2018-2810840.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e35/6311876/46c02da409aa/ECAM2018-2810840.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e35/6311876/df064848d354/ECAM2018-2810840.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e35/6311876/fb93b693b032/ECAM2018-2810840.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e35/6311876/519562ce50fe/ECAM2018-2810840.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e35/6311876/6c1a5c07eab9/ECAM2018-2810840.005.jpg

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