Background

Oxidative stress-induced myoblast damage is one of the major causes of skeletal muscle loss associated with inhibition of myogenic differentiation and muscle dysfunction. Trans-cinnamaldehyde (tCA), the most common essential oil constituent in cinnamon, is known to possess strong anti-oxidant activity. However, it has not been determined whether tCA can protect myoblasts from oxidative damage.

Objectives

The aim of this study was to investigate the protective effect of tCA against oxidative stress-induced damage in mouse myoblast C2C12 cells.

Methods

To examine the efficacy of tCA to protect against oxidative damage, cell viability, morphological changes, DNA damage, mitochondrial membrane potential (MMP) analysis, reactive oxygen species (ROS) generation, and Western blotting were applied.

Results

tCA suppressed hydrogen peroxide (H₂O₂)-induced growth inhibition and DNA damage by blocking abnormal ROS accumulation. In addition, tCA attenuated apoptosis by suppressing loss of MMP and cytosolic release of cytochrome c, increasing the rate of Bcl-2/Bax expression and reducing the activity of caspase-3 in H₂O₂-stimulated cells, suggesting that tCA protected C2C12 cells from mitochondria-mediated apoptosis caused by oxidative stress.

Conclusion

The results showed that tCA may be useful as a potential treatment for the prevention and treatment of various oxidative stress-related muscle disorders in the future.

中文翻译：

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反式肉桂醛通过抑制 ROS 产生来保护 C2C12 成肌细胞免受氧化应激引起的 DNA 损伤、线粒体功能障碍和细胞凋亡。

背景

氧化应激诱导的成肌细胞损伤是与抑制成肌分化和肌肉功能障碍相关的骨骼肌损失的主要原因之一。已知反式肉桂醛 (tCA) 是肉桂中最常见的精油成分，具有很强的抗氧化活性。然而，尚未确定 tCA 是否可以保护成肌细胞免受氧化损伤。

目标

本研究的目的是研究 tCA 对小鼠成肌细胞 C2C12 细胞氧化应激损伤的保护作用。

方法

为了检查 tCA 防止氧化损伤的功效，应用了细胞活力、形态变化、DNA 损伤、线粒体膜电位 (MMP) 分析、活性氧 (ROS) 生成和蛋白质印迹。

结果

tCA 通过阻断异常 ROS 积累来抑制过氧化氢 (H ₂ O ₂ ) 诱导的生长抑制和 DNA 损伤。此外，tCA 通过抑制 MMP 的丢失和细胞色素c的细胞溶质释放、增加 Bcl-2/Bax 表达率和降低 H ₂ O ₂刺激细胞中 caspase-3 的活性来减弱细胞凋亡，表明 tCA 保护了 C2C12氧化应激引起的线粒体介导的细胞凋亡。

结论

结果表明，tCA 可能在未来作为预防和治疗各种氧化应激相关肌肉疾病的潜在治疗方法。