Abstract：
METHODS: Kaempferol (KMP), a bioactive flavonoid compound found in fruits and vegetables, contributes to human health in many ways but little is known about its relationship with muscle mass. The effect of KMP on C2C12 myoblast differentiation and the mechanisms that might underlie that effect are studied.
RESULTS: This study finds that KMP (1, 10 µM) increases the migration and differentiation of C2C12 myoblasts in vitro. Studying the possible mechanism underlying its effect on migration, the study finds that KMP activates Integrin Subunit Beta 1 (ITGB1) in C2C12 myoblasts, increasing p-FAK (Tyr398) and its downstream cell division cycle 42 (CDC42), a protein previously associated with cell migration. Regarding differentiation, KMP upregulates the expression of myosin heavy chain (MHC) and activates IGF1/AKT/mTOR/P70S6K. Interestingly, pretreatment with an AKT inhibitor (LY294002) and siRNA knockdown of IGF1R leads to a decrease in cell differentiation, suggesting that IGF1/AKT activation is required for KMP to induce C2C12 myoblast differentiation.
CONCLUSIONS: Together, the findings suggest that KMP enhances the migration and differentiation of C2C12 myoblasts through the ITG1B/FAK/paxillin and IGF1R/AKT/mTOR pathways. Thus, KMP supplementation might potentially be used to prevent or delay age-related loss of muscle mass and help maintain muscle health.
RESULTS: This study finds that KMP (1, 10 µM) increases the migration and differentiation of C2C12 myoblasts in vitro. Studying the possible mechanism underlying its effect on migration, the study finds that KMP activates Integrin Subunit Beta 1 (ITGB1) in C2C12 myoblasts, increasing p-FAK (Tyr398) and its downstream cell division cycle 42 (CDC42), a protein previously associated with cell migration. Regarding differentiation, KMP upregulates the expression of myosin heavy chain (MHC) and activates IGF1/AKT/mTOR/P70S6K. Interestingly, pretreatment with an AKT inhibitor (LY294002) and siRNA knockdown of IGF1R leads to a decrease in cell differentiation, suggesting that IGF1/AKT activation is required for KMP to induce C2C12 myoblast differentiation.
CONCLUSIONS: Together, the findings suggest that KMP enhances the migration and differentiation of C2C12 myoblasts through the ITG1B/FAK/paxillin and IGF1R/AKT/mTOR pathways. Thus, KMP supplementation might potentially be used to prevent or delay age-related loss of muscle mass and help maintain muscle health.
摘要：
方法：山奈酚（KMP），一种在水果和蔬菜中发现的生物活性类黄酮化合物，在许多方面有助于人类健康，但对它与肌肉质量的关系知之甚少。研究了KMP对C2C12成肌细胞分化的影响以及可能作为该影响基础的机制。
结果：这项研究发现，KMP（1,10µM）在体外增加了C2C12成肌细胞的迁移和分化。研究其对迁移影响的潜在机制，研究发现，KMP激活C2C12成肌细胞中的整合素亚基β1（ITGB1），增加p-FAK（Tyr398）及其下游细胞分裂周期42（CDC42），一种以前与细胞迁移有关的蛋白质。关于差异化，KMP上调肌球蛋白重链（MHC）的表达并激活IGF1/AKT/mTOR/P70S6K。有趣的是,用AKT抑制剂（LY294002）预处理和IGF1R的siRNA敲低导致细胞分化减少，提示IGF1/AKT激活是KMP诱导C2C12成肌细胞分化所必需的。
结论：一起，研究结果表明，KMP通过ITG1B/FAK/桩蛋白和IGF1R/AKT/mTOR途径增强C2C12成肌细胞的迁移和分化。因此，补充KMP可能可能用于预防或延迟与年龄相关的肌肉质量损失，并有助于维持肌肉健康。
结果：这项研究发现，KMP（1,10µM）在体外增加了C2C12成肌细胞的迁移和分化。研究其对迁移影响的潜在机制，研究发现，KMP激活C2C12成肌细胞中的整合素亚基β1（ITGB1），增加p-FAK（Tyr398）及其下游细胞分裂周期42（CDC42），一种以前与细胞迁移有关的蛋白质。关于差异化，KMP上调肌球蛋白重链（MHC）的表达并激活IGF1/AKT/mTOR/P70S6K。有趣的是,用AKT抑制剂（LY294002）预处理和IGF1R的siRNA敲低导致细胞分化减少，提示IGF1/AKT激活是KMP诱导C2C12成肌细胞分化所必需的。
结论：一起，研究结果表明，KMP通过ITG1B/FAK/桩蛋白和IGF1R/AKT/mTOR途径增强C2C12成肌细胞的迁移和分化。因此，补充KMP可能可能用于预防或延迟与年龄相关的肌肉质量损失，并有助于维持肌肉健康。
