Journal
INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
Volume 17, Issue 4, Pages 1138-1152Publisher
IVYSPRING INT PUBL
DOI: 10.7150/ijbs.57825
Keywords
Betulinic acid; autophagy; mitophagy; pyroptosis; spinal cord injury
Categories
Funding
- Zhejiang Provincial Public Welfare Technology Application Research Project [LGF20H150003]
- Zhejiang Provincial Science and Technology Project of Traditional Chinese Medicine [2021ZB183]
- Zhejiang Provincial Medicine and Health Technology Project [2017KY472]
- Natural Science Foundation of China [82072192]
- Zhejiang Provincial Natural Science Foundation of China [LY21H060050]
- Wenzhou Science and Technology Bureau Foundation [Y20190078]
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The study found that betulinic acid has a significant therapeutic effect on spinal cord injury by promoting autophagy and mitophagy to improve functional recovery.
Spinal cord injury (SCI) results in a wide range of disabilities. Its complex pathophysiological process limits the effectiveness of many clinical treatments. Betulinic acid (BA) has been shown to be an effective treatment for some neurological diseases, but it has not been studied in SCI. In this study, we assessed the role of BA in SCI and investigated its underlying mechanism. We used a mouse model of SCI, and functional outcomes following injury were assessed. Western blotting, ELISA, and immunofluorescence techniques were employed to analyze levels of autophagy, mitophagy, pyroptosis, and AMPK-related signaling pathways were also examined. Our results showed that BA significantly improved functional recovery following SCI. Furthermore, autophagy, mitophagy, ROS level and pyroptosis were implicated in the mechanism of BA in the treatment of SCI. Specifically, our results suggest that BA restored autophagy flux following injury, which induced mitophagy to eliminate the accumulation of ROS and inhibits pyroptosis. Further mechanistic studies revealed that BA likely regulates autophagy and mitophagy via the Spinal cord injury (SCI) results in a wide range of disabilities. Its complex pathophysiological process limits the effectiveness of many clinical treatments. Betulinic acid (BA) has been shown to be an effective treatment for some neurological diseases, but it has not been studied in SCI. In this study, we assessed the role of BA in SCI and investigated its underlying mechanism. We used a mouse model of SCI, and functional outcomes following injury were assessed. Western blotting, ELISA, and immunofluorescence techniques were employed to analyze levels of autophagy, mitophagy, pyroptosis, and AMPK-related signaling pathways were also examined. Our results showed that BA significantly improved functional recovery following SCI. Furthermore, autophagy, mitophagy, ROS level and pyroptosis were implicated in the mechanism of BA in the treatment of SCI. Specifically, our results suggest that BA restored autophagy flux following injury, which induced mitophagy to eliminate the accumulation of ROS and inhibits pyroptosis. Further mechanistic studies revealed that BA likely regulates autophagy and mitophagy via the AMPK-mTOR-TFEB signaling pathway. Those results showed that BA can significantly promote the recovery following SCI and that it may be a promising therapy for SCI.
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