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Profiling Alterations of the Metabolomic and Transcriptomic Characteristics and the Therapeutic Mechanism of Psoraleae Fructus in Treating Kidney-Yang Deficiency Syndrome Rats
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Kidney-yang deficiency syndrome (KYDS) is a metabolic disease caused by neuroendocrine disorders often accompanied by abnormal liver function. Psoraleae Fructus (BGZ) is widely used to treat KYDS in China, but it is unclear whether BGZ plays a therapeutic role in regulating liver function. Organ index, ALT, AST, and HE staining were used to evaluate the protective effect of BGZ on KYDS in rats, and transcriptomics and metabolomics were employed to screen for potential biomarkers. The results showed that BGZ treatment significantly decreased the levels of ALT and AST, and ameliorated liver pathological damage in KYDS rats. 92 differentially expressed genes (DEGs) and 20 metabolites were significantly disturbed by BGZ in KYDS rats. Integrated analysis of metabolites and DEGs revealed that neuroactive ligand-receptor interaction, cAMP pathway, calcium signaling pathway, and cytokine-cytokine receptor interaction may be the main mechanism of BGZ treatment, and the key targets of the cAMP pathway were confirmed by ELISA and RT-qPCR. In conclusion, the cAMP pathway may be the partial mechanism by which BGZ exerts protective effects on KYDS, and the study results also lay the foundation for more in-depth mechanistic studies and drug-targeted therapy of KYDS in the future.
Title: Profiling Alterations of the Metabolomic and Transcriptomic Characteristics and the Therapeutic Mechanism of Psoraleae Fructus in Treating Kidney-Yang Deficiency Syndrome Rats
Description:
Kidney-yang deficiency syndrome (KYDS) is a metabolic disease caused by neuroendocrine disorders often accompanied by abnormal liver function.
Psoraleae Fructus (BGZ) is widely used to treat KYDS in China, but it is unclear whether BGZ plays a therapeutic role in regulating liver function.
Organ index, ALT, AST, and HE staining were used to evaluate the protective effect of BGZ on KYDS in rats, and transcriptomics and metabolomics were employed to screen for potential biomarkers.
The results showed that BGZ treatment significantly decreased the levels of ALT and AST, and ameliorated liver pathological damage in KYDS rats.
92 differentially expressed genes (DEGs) and 20 metabolites were significantly disturbed by BGZ in KYDS rats.
Integrated analysis of metabolites and DEGs revealed that neuroactive ligand-receptor interaction, cAMP pathway, calcium signaling pathway, and cytokine-cytokine receptor interaction may be the main mechanism of BGZ treatment, and the key targets of the cAMP pathway were confirmed by ELISA and RT-qPCR.
In conclusion, the cAMP pathway may be the partial mechanism by which BGZ exerts protective effects on KYDS, and the study results also lay the foundation for more in-depth mechanistic studies and drug-targeted therapy of KYDS in the future.
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