Cardiovascular disease (CVD) can arise because of chronic inflammation and inflammatory bowel disease (IBD) is one such disease where the risk for CVD and eventual heart failure is increased considerably. The incidence of IBD, which refers to both ulcerative colitis and Crohn's disease, has been on the increase in several countries and is a potential risk factor for CVD. Although IBD can potentially cause venous thromboembolism, its significance in arterial stiffening, atherosclerosis, ischemic heart disease and myocardial infarction is only being realized now and it is currently under debate. However, several studies with large groups of patients have demonstrated the association of IBD with heart disease. It has been suggested that systemic inflammation as observed in IBD patients leads to oxidative stress and elevated levels of inflammatory cytokines such as tumor necrosis factor-α (TNF-α), which lead to phenotypic changes in smooth muscle cells and sets into motion a series of events that culminate in atherosclerosis and CVD. Besides the endogenous factors and cytokines, it has been suggested that due to the compromised intestinal mucosal barrier, endotoxins and bacterial lipopolysaccharides produced by intestinal microflora can enter into circulation and activate inflammatory responses that lead to atherosclerosis. Therapeutic management of IBD-associated heart diseases cannot be achieved with simple anti-inflammatory drugs such as corticosteroids and anti-TNF-α antibodies. Treatment with existing medications for CVDs, aspirin, platelet aggregation inhibitors and statins is found to be acceptable and safe. Nevertheless, further research is needed to assess their efficacy in IBD patients suffering from heart disease.

Nesfatin-1 may be associated with IBS-like visceral hypersensitivity, which may be implicated in brain CRF/CRF1 signaling pathways.

To study the therapeutic effect of Armillarisin A on patients with ulcerative colitis (UC) and on serum IL-1β and IL-4, sixty patients with UC were randomly divided into three groups: Armillarisin A treatment group (Group I), Armillarisin-combined hormone therapy group (Group II), and hormones treatment as the control group (Group III). Patients in Group I received Armillarisin A 10 mg enema in 100 ml saline. Patients in Group II received Armillarisin A 10 mg and dexamethasone 5 mg enema in 100 ml saline. Patients in Group III received only dexamethasone 5 mg enema in 100 ml saline. The therapeutic efficacy and serum levels of IL-4 and IL-1β were observed. After 4 week treatment, the total effective rates were 90.0 % in Group I and 95.0 % in Group II. Both are higher than it in control group, which was 70.0 %. The serum levels of IL-4 in Groups I and II were significantly higher than it in control group. Compared to IL-4 levels before treatment, the levels of IL-4 after treatment were significantly higher in both Groups I and II. The serum levels of IL-11β were significantly decreased in Groups I and II in comparison to it in control group. Compared to the levels of IL-1β before treatment, the levels of IL-1β were significantly decreased. Armillarisin A shows a significant effect in treating UC. It helps increase IL-4 and lower IL-1β and the mechanism may be related to the body’s immunity regulation.