Modified Sanliangsan improved Sjogren’s syndrome complicated with interstitial lung disease by suppressing serum MUC1 levels

Abstract Objectives To clarify if the mechanism of Sanliangsan in improving Sjogren’s syndrome complicated with interstitial lung disease (SS-ILD) involves MUC1 suppression, which is involved in SS-ILD pathogenesis. Methods Fifty-six patients were randomly divided into two groups receiving Sanliangsan prescription therapy and conventional therapy. In-depth transcriptome profiles collected and analyzed to identify candidate genes involved in SS pathogenesis. Clinical symptom scores, metabolic compositions, lung HRCT scores, and serum MUC1 levels were compared between the two groups before and after treatment. Metabolome analyzed the metabolic composition of serum with SS-ILD before and after SP treatment. Results Transcriptome results identified the involvement of abnormal expression of genes relevant to the immune system, inflammatory responses, and signaling pathways. MUC1 was involved in SS pathogenesis and could be used to diagnose SS-ILD early. The SP therapy improved SS-ILD more effectively than conventional therapy. Moreover, Sanliangsan prescription therapy reduced serum MUC1 levels and restored the abnormal metabolisms, improving the abnormal inflammatory and immune responses of patients. Eugenol directly interacted with MUC1, and suppressed related genes, and was the bioactive compound of SP. Conclusion Modified Sanliangsan can improve the clinical symptoms, signs, and lung function of patients; the mechanism may be due to eugenol and related to MUC1 regulation