Journal of cachexia, sarcopenia and muscle · 2025
Polygonati Rhizoma Prevents Glucocorticoid-Induced Growth Inhibition of Muscle via Promoting Muscle Angiogenesis Through Deoxycholic Acid.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Shi Shiyi, Li Rui, Han Yanxu, Xie Jiahao, Wang Shaoshuai, Liu Jie, Wan Fangyan, Hou Gaifeng, Liu Zuhong, Sun Xiaobo, Zuo Bo, Jia Zhihao, Mei Zhinan, Song Tongxing
Аннотация
BACKGROUND: Glucocorticoids are commonly used in clinical treatments but can cause muscle growth inhibition and weakness at high doses. The mechanisms and treatments for glucocorticoid-induced muscle growth inhibition remain poorly understood. This study aims to investigate the anti-atrophic effects of Polygonati Rhizoma (PR) and a mixture of low-dose fructose and glucose (MFG, an active component mimic in PR) on skeletal muscle.
METHODS: Male C57BL/6 mice (3-week-old, n = 8) were gavaged with aqueous extract of PR (AEPR). MFG was used to gavage normal male C57BL/6 mice (3-week-old, n = 10) and male C57BL/6 mice with dexamethasone (DEX)-induced muscle growth inhibition (3-week-old, n = 7). After 2 weeks of gavage, the body weight and muscle mass of the mice were measured. Intestinal content was collected, the concentration of deoxycholic acid (DCA) was analysed and gut microbiota changes were assessed through 16S rRNA gene sequencing. Muscle angiogenesis was examined through the expression of vascular endothelial growth factors (VEGFs), focusing on the DCA-activated TGR5/cAMP/PKA/pCREB pathway.
RESULTS: AEPR significantly increased the body weight (22.90 ± 0.90 vs. 21.83 ± 0.87 g, *p < 0.05) and grip strength (1.32 ± 0.11 vs. 1.04 ± 0.12 N, ***p < 0.001) of mice. MFG (0.5 g/kg body weight) also significantly elevated the body weight (21.44 ± 0.71 vs. 20.14 ± 0.82 g, **p < 0.01) and muscle mass (0.37 ± 0.018 vs. 0.33 ± 0.035 g, **p < 0.01) of mice. In the DEX group, MFG restored the DCA level (log2[intensity]) in intestinal content (25.41 ± 1.64 vs. 22.69 ± 0.74, *p < 0.05) and increased the abundance of Collinsella aerofaciens as measured by DNA concentration (0.80 ± 0.64 vs. 0.24 ± 0.09 pg/μL, p = 0.096). Mechanistically, MFG upregulated VEGFs expression and promoted muscle angiogenesis via the TGR5/cAMP/PKA/pCREB pathway.
CONCLUSIONS: This study demonstrates that AEPR and its active component mimic MFG can promote muscle growth and MFG mitigates muscle growth inhibition by modulating gut microbiota and enhancing muscle angiogenesis. These findings suggest that fructose-containing treatments are novel strategies to address skeletal muscle dysfunction.
METHODS: Male C57BL/6 mice (3-week-old, n = 8) were gavaged with aqueous extract of PR (AEPR). MFG was used to gavage normal male C57BL/6 mice (3-week-old, n = 10) and male C57BL/6 mice with dexamethasone (DEX)-induced muscle growth inhibition (3-week-old, n = 7). After 2 weeks of gavage, the body weight and muscle mass of the mice were measured. Intestinal content was collected, the concentration of deoxycholic acid (DCA) was analysed and gut microbiota changes were assessed through 16S rRNA gene sequencing. Muscle angiogenesis was examined through the expression of vascular endothelial growth factors (VEGFs), focusing on the DCA-activated TGR5/cAMP/PKA/pCREB pathway.
RESULTS: AEPR significantly increased the body weight (22.90 ± 0.90 vs. 21.83 ± 0.87 g, *p < 0.05) and grip strength (1.32 ± 0.11 vs. 1.04 ± 0.12 N, ***p < 0.001) of mice. MFG (0.5 g/kg body weight) also significantly elevated the body weight (21.44 ± 0.71 vs. 20.14 ± 0.82 g, **p < 0.01) and muscle mass (0.37 ± 0.018 vs. 0.33 ± 0.035 g, **p < 0.01) of mice. In the DEX group, MFG restored the DCA level (log2[intensity]) in intestinal content (25.41 ± 1.64 vs. 22.69 ± 0.74, *p < 0.05) and increased the abundance of Collinsella aerofaciens as measured by DNA concentration (0.80 ± 0.64 vs. 0.24 ± 0.09 pg/μL, p = 0.096). Mechanistically, MFG upregulated VEGFs expression and promoted muscle angiogenesis via the TGR5/cAMP/PKA/pCREB pathway.
CONCLUSIONS: This study demonstrates that AEPR and its active component mimic MFG can promote muscle growth and MFG mitigates muscle growth inhibition by modulating gut microbiota and enhancing muscle angiogenesis. These findings suggest that fructose-containing treatments are novel strategies to address skeletal muscle dysfunction.