在現實生活中，肌肉損傷可能由不適當的運動所引發；而在本實驗裡，為了模擬肌肉損傷，我們透過缺氧的方式，對肌肉纖維母細胞 C2C12 造成氧化壓力；在缺氧的狀況下，活性氧化物（reactive oxygen species, ROS）與脂質活性氧化物（lipid ROS）的堆積會分別誘發細胞凋亡與鐵依賴型細胞死亡並最終導致細胞的死亡。既然氧化壓力是造成細胞損傷與死亡的重要機轉之一，如能在天然植物中找到具備減緩氧化壓力功效之成分，就可能用於減緩肌肉細胞的損傷，而在本研究中，我們選擇了丹參素作為實驗的對象。研究結果發現，丹參素能夠通過調控細胞凋亡的相關因子包含 BCL2、BAX 以及 cleaved-caspase 3（clCASP3），以及鐵依賴型細胞死亡的相關因子包含 GPX4 以及 SLC7A11，分別降低細胞凋亡及鐵依賴型細胞死亡的現象，並藉此保護骨骼肌細胞免於死亡。我們也同時觀察到丹參素的使用能降低活性氧化物與脂質活性氧化物的堆積。對於將丹參素用於骨骼肌細胞的氧化誘發損傷之替代療法，這些研究發現可以提供新的見解。;Exercise-induced muscle damage can be caused by eccentric exercise that is excessive or unaccustomed. For mimicking intracellular muscle injury, hypoxia induces oxidative stress on C2C12 myoblast cells. Under hypoxia, accumulation of ROS and lipid ROS caused cell death via apoptosis and ferroptosis, respectively. The identification of the candidate natural products involved in oxidative stress and the development of strategies to mitigate it have attracted considerable attention. In this study, we use Danshensu as a candidate product to speculate whether it has a protective effect on hypoxia-caused C2C12 cells damage via apoptosis and ferroptosis. Results showed that Danshensu alleviated the cell death and apoptosis via regulations of BCL2, BAX, and clCASP3, as well as ferroptosis via regulations of GPX4 and SLC7A11 upon hypoxia. Moreover, accumulations of ROS and lipid ROS caused by hypoxia were attenuated in presence of Danshensu. These findings may provide new insight into the possibility of Danshensu as an alternative treatment for hypoxia-induced damage to skeletal muscle C2C12 cell line.
