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<p>Glucocorticoids such as dexamethasone (DEX) are commonly used clinically but can induce skeletal muscle atrophy with prolonged or high-dose exposure. <i>Trichosanthes kirilowii</i> Maximowicz (TK), a traditional medicinal herb, has known pharmacological effects, but its impact on muscle atrophy remains unclear. This study investigated the anti-atrophic potential of TK in DEX-induced muscle atrophy models. In C2C12 cells, TK improved cell viability and restored myotube diameter and number, downregulated atrophy markers MuRF-1 and Atrogin-1, and upregulated myogenic markers MyoD, MyoG, and MHC. TK also restored Sirtuin 1 (SIRT1) expression suppressed by DEX, and inhibition of SIRT1 with EX527 reduced TK’s beneficial effects, indicating a SIRT1–dependent mechanism. TK rescued DEX-induced reductions in phosphorylated AKT and mTOR, supporting its role in muscle anabolism. In vivo, oral TK administration attenuated DEX-induced weight loss, preserved gastrocnemius muscle mass, and improved motor performance. Molecular docking analysis revealed that key TK-derived compounds, including 5-dehydrokarounidiol, steryl glucoside, and isomultiflorenol, exhibited moderate binding affinity (− 6.3 to − 6.6&#xa0;kcal/mol) toward the allosteric site of SIRT1. These findings suggest that TK protects against muscle atrophy by modulating SIRT1–related anabolic and catabolic pathways. TK may offer therapeutic potential for sarcopenia and glucocorticoid-induced muscle wasting.</p>

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Trichosanthes kirilowii Maximowicz attenuates dexamethasone induced atrophy in C2C12 myotubes through a Sirtuin 1 associated mechanism

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月24日

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  • Hyunseong Kim,
  • Jin Young Hong,
  • Changhwan Yeo,
  • Wan-Jin Jeon,
  • Hyun Kim,
  • Junseon Lee,
  • Yoon Jae Lee,
  • In-Hyuk Ha

摘要

Glucocorticoids such as dexamethasone (DEX) are commonly used clinically but can induce skeletal muscle atrophy with prolonged or high-dose exposure. Trichosanthes kirilowii Maximowicz (TK), a traditional medicinal herb, has known pharmacological effects, but its impact on muscle atrophy remains unclear. This study investigated the anti-atrophic potential of TK in DEX-induced muscle atrophy models. In C2C12 cells, TK improved cell viability and restored myotube diameter and number, downregulated atrophy markers MuRF-1 and Atrogin-1, and upregulated myogenic markers MyoD, MyoG, and MHC. TK also restored Sirtuin 1 (SIRT1) expression suppressed by DEX, and inhibition of SIRT1 with EX527 reduced TK’s beneficial effects, indicating a SIRT1–dependent mechanism. TK rescued DEX-induced reductions in phosphorylated AKT and mTOR, supporting its role in muscle anabolism. In vivo, oral TK administration attenuated DEX-induced weight loss, preserved gastrocnemius muscle mass, and improved motor performance. Molecular docking analysis revealed that key TK-derived compounds, including 5-dehydrokarounidiol, steryl glucoside, and isomultiflorenol, exhibited moderate binding affinity (− 6.3 to − 6.6 kcal/mol) toward the allosteric site of SIRT1. These findings suggest that TK protects against muscle atrophy by modulating SIRT1–related anabolic and catabolic pathways. TK may offer therapeutic potential for sarcopenia and glucocorticoid-induced muscle wasting.