Figure 7.
The hypothetical model of Clostridium butyricum protective effect on gastric ulcers induced by stressful stimuli. In addition to competitive inhibition of Helicobacter pylori, as reported by previous studies[17], Clostridium butyricum (C. butyricum) protects gastric mucosa from lesions through at least two different mechanisms: anti-oxidation and anti-inflammation. The metabolites of C. butyricum, such as butyrate and hydrogen[52], enhance the activity of antioxidases [superoxide dismutase (SOD) and catalase (CAT)], reduce the production of proinflammatory factors [interleukin (IL)-1β, tumor necrosis factor (TNF)-α, leukotriene B4 (LTB4)] and promote the production of anti-inflammatory prostaglandins (PGI2), thus exerting protective effect on gastric ulcers by resolving peroxidation and alleviating exaggerated inflammation induced by various stresses.