数据日期 2026-10-29 · 生成时间 2026-10-29 06:03
研究问题
Therefore, this study aimed to investigate the effects of Rg2 on sarcopenia in aged male mice and its potential molecular mechanisms of action.
方法
We analyzed genes and counted the features of each sample, filtering out cells with fewer than 500 or more than 4500 detected genes, as well as cells with mitochondrial contamination exceeding 5%.；Subsequently, we explored the correlation between appendicular skeletal muscle mass index and age across the sexes. re randomly divided into five groups (n = 8): the aging (Old), low-dose Rg2 (Rg2-L; G107680, Aladdin, US), medium-dose Rg2 (Rg2-M), high-dose Rg2 (Rg2-H), and nicotinamide mononucleotide (NMN; N1492501, Aladdin, US) groups.；Solvent correction and noise reduction were performed when necessary to minimize experimental artifacts. e target stability (DARTS) For the CETSA, muscle lysates were treated with dimethyl sulfoxide or Rg2 (100 μM) for 3 h at 4°C.；The data are presented as mean ± SD. on Omnibus (GEO) database, we performed UMAP analysis (Fig.
核心结论
Statistical data are presented as the mean ± SD (P < 0.01, P < 0.0001).；Statistical data are presented as the mean ± SD (*P < 0.05, P < 0.01, *P < 0.001, P < 0.0001). ‖ 结论**：In conclusion, this study suggests that Rg2 improves aging-related skeletal muscle dysfunction and fibrotic remodeling in aged male mice, at least partly in association with attenuation of TGF-β1/Smad signaling.
局限
Through multidimensional approaches, including multi-database analysis, in vivo and in vitro experiments, and molecular interaction assays, this study provides preliminary evidence that Rg2 interacts with TGF-β1 and attenuates downstream TGF-β1/Smad signaling activation, thereby improving muscle mass, muscle function, and aging-related fibrotic remodeling in aged male mice.；However, whether Rg2 directly interferes with TGF-β1 binding to TGFBR1/TGFBR2 remains to be determined.；Although this study provides preliminary evidence supporting the protective effects of Rg2 against aging-related skeletal muscle dysfunction and fibrotic remodeling, several limitations should be acknowledged.
对本项目的价值
★★★☆☆ 衰弱/肌少症是少有的已有监管认可终点的老年综合征，是临床转化的最短路径。队列：NHANES、CHARLS；最大样本量约 8；设计 孟德尔随机化、前瞻队列。
全文来源
PMC JATS 全文（正文 53,611 字符，已过标题/DOI 逐字归属校验）
原文题录
- 英文标题：Ginsenoside Rg2 attenuates TGF-β1/Smad-mediated fibrotic remodeling in aged male mice with sarcopenia.
- 期刊与标识：J Ginseng Res · PMID 42948583 · DOI 10.1016/j.jgr.2026.101115**
B 级证据分级：B 级（同行评议临床前研究，主要为动物模型）
本文核心结论来自动物模型或体外细胞学，属临床前证据，不能外推至人体。「延长健康寿命」「改善功能」等表述在小鼠中的意义，与人类临床结局之间仍有距离。
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