Phytomedicine : international journal of phytotherapy and phytopharmacology · 2024
Study on the anti-Parkinson's disease activity mechanism and preparation of panaxadiol.
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Xu Lei, Zhang Zhongjin, Feng Ziqi, Niu Sixiang, Yang Lixia, Xiao Baoguo, Jin Xiao-Ming, Ma Cungen, Fan Huijie, Xiao Shengnan, Chai Zhi
Аннотация
BACKGROUND: Traditional Chinese medicine offers unique and valuable resources for the exploration of novel approaches to disease treatment. Panaxadiol, an active compound derived from the transformation of ginsenosides. It has a variety of pharmacological activities. However, there is a lack of research regarding its effects on Parkinson's disease (PD).
PURPOSE AND STUDY DESIGN: This study investigates the activity and mechanism of panaxadiol in the treatment of PD both in vivo and in vitro. In addition, a new method has been developed to extract panaxadiol.
RESULTS: The results showed that in vitro, panaxadiol can reduce the viability and cytotoxicity of BV2 cells induced by LPS, and inhibit the production of pro-inflammatory factors through the TLR4/MyD88/NF-κB pathway. In vivo, panaxadiol can improve motor and intestinal dysfunction in PD mice and repair the loss of DA neurons. Further studies have shown that panaxadiol treatment alleviates damage to the blood-brain barrier (BBB), inhibits neuroinflammation in the substantia nigra (SN), and further reduces damage to DA neurons. Subsequently, it was found that panaxadiol alleviated peripheral inflammation and significantly restored the intestinal microbial community. Further mechanistic studies found that panaxadiol treatment inhibited the TLR4/MyD88/NF-κB signaling pathway and its downstream pro-inflammatory products in the SN. In addition, Additionally, the response surface method was employed to identify the optimal conditions for extracting panaxadiol using a deep eutectic solvent (NADES).
CONCLUSION: In summary, this study has found for the first time that panaxadiol can effectively improve the symptoms of PD by regulating neuroinflammation, repairing the BBB, and gut microbiota. Meanwhile, adopting a green extraction process significantly increases the content of panaxadiol, providing a new direction for the development of PD candidate drugs.
PURPOSE AND STUDY DESIGN: This study investigates the activity and mechanism of panaxadiol in the treatment of PD both in vivo and in vitro. In addition, a new method has been developed to extract panaxadiol.
RESULTS: The results showed that in vitro, panaxadiol can reduce the viability and cytotoxicity of BV2 cells induced by LPS, and inhibit the production of pro-inflammatory factors through the TLR4/MyD88/NF-κB pathway. In vivo, panaxadiol can improve motor and intestinal dysfunction in PD mice and repair the loss of DA neurons. Further studies have shown that panaxadiol treatment alleviates damage to the blood-brain barrier (BBB), inhibits neuroinflammation in the substantia nigra (SN), and further reduces damage to DA neurons. Subsequently, it was found that panaxadiol alleviated peripheral inflammation and significantly restored the intestinal microbial community. Further mechanistic studies found that panaxadiol treatment inhibited the TLR4/MyD88/NF-κB signaling pathway and its downstream pro-inflammatory products in the SN. In addition, Additionally, the response surface method was employed to identify the optimal conditions for extracting panaxadiol using a deep eutectic solvent (NADES).
CONCLUSION: In summary, this study has found for the first time that panaxadiol can effectively improve the symptoms of PD by regulating neuroinflammation, repairing the BBB, and gut microbiota. Meanwhile, adopting a green extraction process significantly increases the content of panaxadiol, providing a new direction for the development of PD candidate drugs.