Modified Sanliangsan Improved Sjogren's Syndrome Complicated with Interstitial Lung Disease by Suppressing Serum MUC1 Levels

Lihui Tan; Wang Lv; Yuqi Chen; Jianjian Dong; Dun Mao; Rong Wei

doi:10.1021/acsomega.4c01147

Modified Sanliangsan Improved Sjogren's Syndrome Complicated with Interstitial Lung Disease by Suppressing Serum MUC1 Levels

ACS Omega. 2024 Jul 5;9(28):30392-30403. doi: 10.1021/acsomega.4c01147. eCollection 2024 Jul 16.

Authors

Lihui Tan¹, Wang Lv², Yuqi Chen¹, Jianjian Dong¹, Dun Mao³, Rong Wei¹

Affiliations

¹ Department of Rheumatology and Immunology, The People's Hospital of Suzhou New District, Suzhou 215000, China.
² Department of Traditional Chinese Medicine, The Cangzhou central Hospital, Cangzhou 061000, China.
³ Department of Orthopaedic, Community Health Service Center of Suzhou Science and Technology City, Suzhou 215000, China.

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 (SP) therapy and conventional therapy (western medicine). In-depth transcriptome profiles from a large database of SS-ILD patients were collected and analyzed to identify candidate genes involved in SS pathogenesis. Clinical symptom scores, metabolic compositions, lung HRCT (high-resolution computed tomography) scores, and serum MUC1 levels were compared between the two groups before and after treatment. Network pharmacology, molecular docking, and ITC assays were performed to identify bioactive compounds of SP in improving SS. Metabolome analyzed the metabolic composition of serum associated 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. Numerous genes, including CD58, CD86, CTLA4, CXCL8, STAT1, and especially MUC1, were involved in SS pathogenesis and could be used to diagnose SS-ILD early. Both treatments improved the lung HRCT scores and clinical symptoms of SS-ILD. 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, suppressed related genes, and was the bioactive compound of SP. SP could partially restore the abnormal metabolisms associated with SS-ILD pathogenesis.

Conclusion: Based on conventional Western medicine treatment, modified Sanliangsan can significantly improve the clinical symptoms, signs, and lung function of patients; the mechanism may be due to eugenol and related to MUC1 regulation.