Integrated network pharmacology and metabolomics reveal the mechanisms of Jasminum elongatum in anti-ulcerative colitis

Abstract

Jasminum elongatum (JE), an ethnic Chinese medicine, is widely used in the Lingnan region of China, because of its analgesic and antidiarrheal action, as well as its anti-inflammatory effects in gastrointestinal diseases. However, whether JE could against ulcerative colitis (UC) remains unclear. This research aims to reveal JE in treating UC and clarify the underlying mechanism. We used the 2.5% dextran sulfate sodium (DSS)-induced UC mice (C57BL/6J) to evaluate the therapeutic effects of JE. Metabolomics of serum and network pharmacology were combined to draw target-metabolite pathways. Apart from that, the targets of associated pathways were confirmed, and the mechanism of action was made clear, using immunohistochemistry. The pharmacodynamic results, including disease activity index (DAI), histological evaluation, and inflammatory cytokines in colon tissues, demonstrated that JE significantly relieved the physiological and pathological symptoms of UC. Network pharmacology analysis indicated 25 core targets, such as TNF, IL-6, PTGS2 and RELA, and four key pathways, including the NF-κB signaling pathway and arachidonic acid metabolism pathway, which were the key connections between JE and UC. Metabolomics analysis identified 45 endogenous differential metabolites and 9 metabolic pathways by enrichment, with the arachidonic acid metabolism pathway being the main metabolism pathway, consistent with the prediction of network pharmacology. IκB, p65 and COX-2 were identified as key targets and this study demonstrated for the first time that JE reverses 2.5% DSS-induced UC in mice via the IκB/p65/COX-2/arachidonic acid pathway. This study reveals the complex mechanisms underlying the therapeutic effects of JE on UC and provides a new approach to identifying the underlying mechanisms of the pharmacological action of Chinese natural medicines such as JE.

6-Gingerol ameliorates ulcerative colitis by inhibiting ferroptosis based on the integrative analysis of plasma metabolomics and network pharmacology

“…47 Moreover, the expression of ALOX15 was proved to be regulated by PTGS2, which was also regarded as an important hallmark of ferroptosis. 21,55 What is more, it was demonstrated that 6-G could repress PTGS2, which was highly expressed in UC mice. 8 The findings of this study showed that the expression levels of ALOX5, ALOX15, and PTGS2 were notably increased in UC patients and that 6-G had favorable binding activity to these targets.…”

Potential mechanism of tea for treating osteoporosis, osteoarthritis, and rheumatoid arthritis

“…According to the report, TIMP1, PTGS2, ICAM1, MMP9, IL1B, CXCL8, IL-6, and RELA were identified as hub genes in ulcerative colitis ( 109 ), which had been found in the target collection of tea components. A new study, processed by integrating network pharmacology and metabolomics, demonstrated that Jasminum elongatum reverses ulcerative colitis in mice via the IκB/p65/COX-2/arachidonic acid pathway ( 110 ). The tea aqueous extract inhibited experimentally induced colitis and liver injury in mice ( 111 ).…”