Investigating the mechanism of action of Qianlie Jindan tablets in rats with chronic prostatitis using non-targeted metabolomics.

OBJECTIVE

To explore the mechanism of action of Qianlie Jindan tablets by analyzing the metabolomic changes in prostate tissues obtained from rats with chronic prostatitis/chronic pelvic pain (CP/CPPS).

MATERIALS AND

METHODS

Male SD rats were randomly divided into three groups: blank control (BC), model control (MC), and treatment (QLJD) groups, with 10 rats in each group. The model was induced using Complete Freund's adjuvant (CFA) and prostate protein purification solution, and the corresponding drug intervention was given. At the end of the experiment, pathological changes in the prostate tissues were observed using hematoxylin and eosin (HE) staining. Differential metabolites were determined by ultra-high-performance liquid chromatography and tandem electrostatic field orbital trap mass spectrometry (UHPLC-Q Exactive HFX), and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway annotation was performed. The results were then verified by quantitative real-time polymerase chain reaction (PCR).

RESULTS

QLJD reversed the histopathological damage induced by CP/CPPS. Metabolomics analysis showed that UDP-GlcNAc was the key differential metabolite, and can activate the PI3K/AKT/mTOR pathway. The PCR analysis revealed that the mRNA expression levels of PI3K, AKT and mTOR in the MC group were significantly lower than those in the BC group (P < 0.05). These parameters were increased in the QLJD group compared to the MC group (P < 0.05), validating our metabolomics results.

CONCLUSION

QLJD exerts a therapeutic effect on CP/CPPS by activating the PI3K/AKT/mTOR pathway through the regulation of UDP-GlcNAc levels.