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<p>This study aimed to evaluate the protective effects of hydrolyzed <i>Gryllus bimaculatus</i> extract (GBE) against dexamethasone (DEX)-induced sarcopenia in C57BL/6 mice. Muscle atrophy was induced by intraperitoneal injection of DEX (20&#xa0;mg/kg/day) for 10 consecutive days (Day 3–12). GBE (100 or 200&#xa0;mg/kg/day) was administered orally starting 2&#xa0;days before DEX treatment and continued for 12&#xa0;days (Day 1–12). GBE significantly attenuated DEX-induced reductions in body weight and muscle mass. Furthermore, GBE administration upregulated the expression of muscle regeneration–related factors, including IGF-1, mTOR, MyoD, MYF5, and MYF6, while downregulating muscle atrophy markers such as myostatin, FOXO3a, MuRF1, and MAFbx. In addition, GBE enhanced antioxidant enzyme activities and suppressed pro-inflammatory cytokines including IL-6 and TNF-α. These findings suggest that GBE may serve as a promising functional ingredient to prevent glucocorticoid-induced muscle atrophy and may offer therapeutic potential for the management of muscle wasting conditions.</p>

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Protective effects of hydrolyzed Gryllus bimaculatus extract on dexamethasone-induced sarcopenia in C57BL/6 mice

  • 期刊论文

  • 发表日期：

    2026年3月18日

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  • Jae Young Shin,
  • Ji Hyeon Park,
  • Jun Hyeong Lim,
  • Byoung Ok Cho,
  • Ju Seog Kang,
  • Seon Il Jang

摘要

This study aimed to evaluate the protective effects of hydrolyzed Gryllus bimaculatus extract (GBE) against dexamethasone (DEX)-induced sarcopenia in C57BL/6 mice. Muscle atrophy was induced by intraperitoneal injection of DEX (20 mg/kg/day) for 10 consecutive days (Day 3–12). GBE (100 or 200 mg/kg/day) was administered orally starting 2 days before DEX treatment and continued for 12 days (Day 1–12). GBE significantly attenuated DEX-induced reductions in body weight and muscle mass. Furthermore, GBE administration upregulated the expression of muscle regeneration–related factors, including IGF-1, mTOR, MyoD, MYF5, and MYF6, while downregulating muscle atrophy markers such as myostatin, FOXO3a, MuRF1, and MAFbx. In addition, GBE enhanced antioxidant enzyme activities and suppressed pro-inflammatory cytokines including IL-6 and TNF-α. These findings suggest that GBE may serve as a promising functional ingredient to prevent glucocorticoid-induced muscle atrophy and may offer therapeutic potential for the management of muscle wasting conditions.