Abstract：
BACKGROUND: Peucedanum japonicum Thunb. (PJ) is a vegetable widely consumed in East Asia and is known to have anticancer and anti-inflammatory effects. However, the effect of PJ on muscle atrophy remains elusive.
OBJECTIVE: This study aimed to investigate the effect of PJ and its active compound on dexamethasone (DEX)-induced muscle atrophy.
METHODS: We performed qualitative and quantitative analysis of PJ using ultra-performance liquid chromatography-mass spectrometry tandem mass spectrometry (UPLC-MS/MS) and high-performance liquid chromatography (HPLC), respectively. The efficacy of PJ and its main compound 4-caffeoylquinic acid (CQA) on muscle atrophy was evaluated in DEX-induced myotube atrophy and DEX-induced muscle atrophy in mouse myoblasts (C2C12) and C57BL/6 mice, in vitro and in vivo, respectively.
RESULTS: The UPLC-MS/MS and HPLC data showed that the concentration of 4-CQA in PJ was 18.845 mg/g. PJ and 4-CQA treatments significantly inhibited DEX-induced myotube atrophy by decreasing protein synthesis and glucocorticoid translocation to the nucleus in C2C12 myotubes. In addition, PJ enhanced myogenesis by upregulating myogenin and myogenic differentiation 1 in C2C12 cells. PJ supplementation effectively increased muscle function and mass, downregulated atrogenes, and decreased proteasome activity in C57BL/6 mice. Additionally, PJ effectively decreased the nuclear translocation of forkhead transcription factor 3 alpha by inhibiting glucocorticoid receptor.
CONCLUSIONS: Overall, PJ and its active compound 4-CQA alleviated skeletal muscle atrophy by inhibiting protein degradation. Hence, our findings present PJ as a potential novel pharmaceutical candidate for the treatment of muscle atrophy.
OBJECTIVE: This study aimed to investigate the effect of PJ and its active compound on dexamethasone (DEX)-induced muscle atrophy.
METHODS: We performed qualitative and quantitative analysis of PJ using ultra-performance liquid chromatography-mass spectrometry tandem mass spectrometry (UPLC-MS/MS) and high-performance liquid chromatography (HPLC), respectively. The efficacy of PJ and its main compound 4-caffeoylquinic acid (CQA) on muscle atrophy was evaluated in DEX-induced myotube atrophy and DEX-induced muscle atrophy in mouse myoblasts (C2C12) and C57BL/6 mice, in vitro and in vivo, respectively.
RESULTS: The UPLC-MS/MS and HPLC data showed that the concentration of 4-CQA in PJ was 18.845 mg/g. PJ and 4-CQA treatments significantly inhibited DEX-induced myotube atrophy by decreasing protein synthesis and glucocorticoid translocation to the nucleus in C2C12 myotubes. In addition, PJ enhanced myogenesis by upregulating myogenin and myogenic differentiation 1 in C2C12 cells. PJ supplementation effectively increased muscle function and mass, downregulated atrogenes, and decreased proteasome activity in C57BL/6 mice. Additionally, PJ effectively decreased the nuclear translocation of forkhead transcription factor 3 alpha by inhibiting glucocorticoid receptor.
CONCLUSIONS: Overall, PJ and its active compound 4-CQA alleviated skeletal muscle atrophy by inhibiting protein degradation. Hence, our findings present PJ as a potential novel pharmaceutical candidate for the treatment of muscle atrophy.
摘要：
背景：日本前香菜.（PJ）是一种在东亚广泛食用的蔬菜，已知具有抗癌和抗炎作用。然而,PJ对肌肉萎缩的影响仍然难以捉摸。
目的：本研究旨在研究PJ及其活性化合物对地塞米松（DEX）诱导的肌肉萎缩的影响。
方法：我们使用超高效液相色谱-质谱串联质谱（UPLC-MS/MS）和高效液相色谱（HPLC）对PJ进行了定性和定量分析，分别。在DEX诱导的肌管萎缩和DEX诱导的小鼠成肌细胞（C2C12）和C57BL/6小鼠的肌肉萎缩中评估了PJ及其主要化合物4-咖啡酰基奎尼酸（CQA）对肌肉萎缩的功效，在体外和体内，分别。
结果：UPLC-MS/MS和HPLC数据显示，PJ中4-CQA的浓度为18.845mg/g。PJ和4-CQA处理通过减少C2C12肌管中的蛋白质合成和糖皮质激素向细胞核的转运来显著抑制DEX诱导的肌管萎缩。此外,PJ通过上调C2C12细胞中的肌原蛋白和肌原分化1来增强肌生成。补充PJ有效增加肌肉功能和质量，降调节的atrogenes，C57BL/6小鼠的蛋白酶体活性降低。此外,PJ通过抑制糖皮质激素受体有效降低叉头转录因子3α的核易位。
结论：总体而言，PJ及其活性化合物4-CQA通过抑制蛋白质降解减轻骨骼肌萎缩。因此，我们的发现表明PJ是治疗肌肉萎缩的潜在新型候选药物.
目的：本研究旨在研究PJ及其活性化合物对地塞米松（DEX）诱导的肌肉萎缩的影响。
方法：我们使用超高效液相色谱-质谱串联质谱（UPLC-MS/MS）和高效液相色谱（HPLC）对PJ进行了定性和定量分析，分别。在DEX诱导的肌管萎缩和DEX诱导的小鼠成肌细胞（C2C12）和C57BL/6小鼠的肌肉萎缩中评估了PJ及其主要化合物4-咖啡酰基奎尼酸（CQA）对肌肉萎缩的功效，在体外和体内，分别。
结果：UPLC-MS/MS和HPLC数据显示，PJ中4-CQA的浓度为18.845mg/g。PJ和4-CQA处理通过减少C2C12肌管中的蛋白质合成和糖皮质激素向细胞核的转运来显著抑制DEX诱导的肌管萎缩。此外,PJ通过上调C2C12细胞中的肌原蛋白和肌原分化1来增强肌生成。补充PJ有效增加肌肉功能和质量，降调节的atrogenes，C57BL/6小鼠的蛋白酶体活性降低。此外,PJ通过抑制糖皮质激素受体有效降低叉头转录因子3α的核易位。
结论：总体而言，PJ及其活性化合物4-CQA通过抑制蛋白质降解减轻骨骼肌萎缩。因此，我们的发现表明PJ是治疗肌肉萎缩的潜在新型候选药物.
