Translated Abstract
ABSTRACT
Background:
Cistanche tubulosa, a Chinese herbal medicine, has been reported to play a role in anti-aging and anti-fatigue, improving kidney function, enhancing memory and regulating immune system. Paticularly, recent studies revealed that Cistanche tubulosa products show a beneficial effect on restoring exercise-induced fatigue. However, the underlying mechanism remains largely unkown.
Purpose and significance:
The aim of this study is to investigate the molecular mechanism of Cistanche tubulosa extract (CIS) against muscle injury. We used tumor necrosis factor α (TNFα)-induced myoblast injury model to explore the mechanism of CIS. The effects of CIS and its three main components, echinacoside, verbascoside and isoacteoside were also explored. This study elucidated the underlying mechanism of CIS on TNFα-induced myoblast injury, and provided experimental basis and theoretical support for the application of CIS.
Methods and results:
In this study, C2C12 myocytes were treated with 10 ng/mL TNFα during differentiation for 4 days to establish damage model, which is used to determine the effect of CIS on myoblast injury. Our results showed that: 1) TNFα led to a significant myoblast injury, indicated by decrease in cell viability and mitochondrial membrane potential (MMP), as well as accumulation of intracellular reactive oxygen species (ROS). 2) Pretreatment with CIS significantly restored the decrease in cell viability and increase in intracellular ROS. 3) By further analysing the biological effects of Cistanche tubulosa extract, we found that CIS pretreatment alleviated TNFα-induced myotube apoptosis through improving mitochondrial function and relieving oxidative stress. 4) By preliminary screening of the three major components of CIS, we found that isoacteoside significantly ameliorated TNFα-induced decrease of cell viability and accumulation of ROS in C2C12 myotubes. Furthermore, 100 μg/mL isoacteoside effectively improved the decrease of MMP in C2C12 myotubes.
Conclusions:
Our findings showed that CIS pretreatment could enhance mitochondrial function, alleviate oxidative stress, and thus inhibit apoptosis pathway to ameliorate TNFα-induced C2C12 myoblasts damage. Moreover, isoacteoside may be the active ingredient of Cistanche tubulosa extract.
Corresponding authors email
