Journal of ethnopharmacology · 2025
Guiqi Huoxue capsule alleviates cervical spondylosis in rats: Insights from 16S rRNA sequencing, lipidomics, and network pharmacology.
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Tang Hongguang, Ni Wenting, Niu Dejun, Wang Kun, Shen Mengmeng, Meng Fanqiang, Cui Deyu, Zeng Zhen, Sun Chenghong, Shen Jinyang, Li Shirong, Zhou Yue
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Cervical spondylosis (CS) is a common condition primarily caused by intervertebral disc degeneration (IVDD), adversely affecting quality of life. Traditional Chinese medicine believes that Qi deficiency and blood stasis are the main pathogenesis of CS. Guiqi Huoxue capsule (GQHX) has the effect of beneficial Qi tonifying kidneys and promoting blood circulation, which is mainly used in the clinical treatment of CS (Qi deficiency and blood stasis syndrome). However, the underlying mechanism of action has not been reported and clarified.
AIM OF THE STUDY: The aim of this study was to investigate the efficacy and underlying mechanisms of GQHX in CS rats.
MATERIALS AND METHODS: The CS rat model (Qi deficiency and blood stasis syndrome) was established by using IVDD and Ovariectomy (OVX) surgeries, along with qi deficiency and blood stasis modeling. The effects of GQHX on CS rats were evaluated by behavioral tests, blood indexes, H&E staining, and other means. Fatty acid profiles and gut microbiota were analyzed using lipidomics and 16S rRNA sequencing. The mechanism of action of GQHX was investigated by network pharmacology and western blotting.
RESULTS: GQHX reduced the symptoms of CS rats as confirmed by behavioral indicators, serum markers, and other measures of efficacy. Meanwhile, 16S rRNA sequencing and lipidomics results showed that GQHX regulated the abundance of Blautia and Muribaculaceae, influencing the production of various fatty acids (e.g. isobutyric, isovaleric, and linoleic acids). More importantly, network pharmacology and Western blot results suggested that GQHX could alleviate the clinical symptoms of CS by regulating the abnormal expression of AGE-RAGE, MAPK, and HIF-1 signaling pathways.
CONCLUSION: This study elucidated the role of GQHX in alleviating CS and highlighted the mechanisms involved, particularly the regulation of gut microbiota and lipid metabolism, as well as the AGE-RAGE, MAPK, and HIF-1 signaling pathways.
AIM OF THE STUDY: The aim of this study was to investigate the efficacy and underlying mechanisms of GQHX in CS rats.
MATERIALS AND METHODS: The CS rat model (Qi deficiency and blood stasis syndrome) was established by using IVDD and Ovariectomy (OVX) surgeries, along with qi deficiency and blood stasis modeling. The effects of GQHX on CS rats were evaluated by behavioral tests, blood indexes, H&E staining, and other means. Fatty acid profiles and gut microbiota were analyzed using lipidomics and 16S rRNA sequencing. The mechanism of action of GQHX was investigated by network pharmacology and western blotting.
RESULTS: GQHX reduced the symptoms of CS rats as confirmed by behavioral indicators, serum markers, and other measures of efficacy. Meanwhile, 16S rRNA sequencing and lipidomics results showed that GQHX regulated the abundance of Blautia and Muribaculaceae, influencing the production of various fatty acids (e.g. isobutyric, isovaleric, and linoleic acids). More importantly, network pharmacology and Western blot results suggested that GQHX could alleviate the clinical symptoms of CS by regulating the abnormal expression of AGE-RAGE, MAPK, and HIF-1 signaling pathways.
CONCLUSION: This study elucidated the role of GQHX in alleviating CS and highlighted the mechanisms involved, particularly the regulation of gut microbiota and lipid metabolism, as well as the AGE-RAGE, MAPK, and HIF-1 signaling pathways.