Abstract
Purpose:
The molecular basis underlying the clinical differentiation in treating psoriasis with syndromes of blood-heat or blood-stasis in traditional Chinese medicine remains unclear. This study employs an integrated multi-omics approach to explore the similarities and differences in the pathogenic mechanisms of these two syndromes, and to elucidate the molecular foundations of Compound Qingdai Capsule and Yinxiekang Pian, which are representative formulas for syndrome-specific treatment, thereby providing insights into the scientific connotation of syndrome differentiation and treatment.
Methods:
Multi-omics data were integrated with machine learning to identify genes differentiating the two syndromes of psoriasis. The therapeutic mechanisms were explored through network pharmacology and molecular docking. Finally, in vivo experiments involved constructing composite psoriasis models in SD rats by combining traditional Chinese medicine syndromes with imiquimod induction, and analyzing skin lesion tissues via qPCR and ELISA.
Results:
After constructing the psoriasis pathway network and successfully establishing rat models, the research identified the characteristic genes of blood-heat syndrome psoriasis as GSK3B, MTOR and CDK4, and those of blood-stasis syndrome psoriasis as AKT1, TNF and STAT3. STAT1 was found to be a common characteristic gene of both syndromes, while LTBP1, PROS1, and ALDH16A1 were the differential genes for distinguishing the two syndromes. Finally, Compound Qingdai Capsule and Yinxiekang Pian were shown to reduce the mRNA and protein expressions of GSK3B, AKT1 and STAT1 to varying degrees.
Conclusion:
GSK3B and AKT1 are differentially expressed in blood-heat syndrome and blood-stasis syndrome psoriasis respectively, while STAT1 is a common inflammatory mediator for both. Compound Qingdai Capsule and Yinxiekang Pian respectively provide a theoretical basis for traditional Chinese medicine syndrome differentiation and treatment of psoriasis by intervening in the same or different inflammatory targets and signaling pathways.
Keywords:
blood-heat syndrome; blood-stasis syndrome; multi-omics analysis; psoriasis; syndrome differentiation and treatment.