## 4 Discussion
The results of the present study also indicate that this improved Shuidouchi fermentation could prevent colitis by regulating the expression levels of nNOS, eNOS, and iNOS in the colon. Colitis occurs in response to colon dysfunction and a decline in colon motility; furthermore, colitis can also cause a decrease in the number of normal interstitial Cajal cells, thus reducing colon motility, which is directly related to colitis [44]. C-Kit can maintain the number of interstitial Cajal cells and prevent the aggravation of colitis [45]. SCF also plays an important role in maintaining the number of interstitial Cajal cells. The number of interstitial Cajal cells decreases and their proliferation is affected by the impaired inflammation of the SCF/Kit signal pathway, which further aggravates colitis [44]. These results showed that enhanced expression of c-Kit and SCF mRNA in the colon could alleviate colitis and thus, Shuidouchi could prevent colitis. Simultaneously, the effects of high-concentration Shuidouchi were close to those of sulfasalazine, which is the main drug used to treat colitis. A large number of inflammatory cells, including neutrophils and lymphocytes, were recruited into the injured tissues during the UC active phase [46]. Immune cells overcame the vascular endothelial cell barrier moving between the body fluids and tissues and involving many steps that are required for cells that flow with the body fluid. Cells are firmly adhered to the blood vessel endothelium, and the cells pass through the intercellular space of the endotheliocyte. Cells then migrate to specific tissues. During this process, cell selectivity and stable adhesion of selected cells are observed. Apart from activating and chemoattracting inflammatory cells, chemokines with increased expression can also trigger other complex inflammatory activities, such as exocytosis, the production of metalloproteinase-degrading matrix, and upregulation of oxidative bursts [47]. Chemokines control the exudation of IL-8 via intracellular signal transduction, which is a typical neutrophil chemokine and activator that mediates inflammatory responses in various ways, including colitis [48]. CINC-1 is a neutrophil chemokine of the IL-8 family, while CXCR2 is a receptor for CINC-1. CXCR2 acts as a mediator to regulate organ-to-organ interactions. Decreasing the expression of CXCR2 in tissues can effectively reduce colonic tissue damage that is caused by colitis [49]. Therefore, the experimental results indicate that Shuidouchi can inhibit colitis by downregulating the expression of CXCR2 and IL-8. IL-6 is also known as proinflammatory cytokine and it is a widely used cytokine. It can affect inflammation, host defense, and tissue damage through humoral and cellular immune functions. Its production can be regulated by IL-1, interferon, and TNF-\(\alpha\)[50]. IL-12 is an inflammatory cytokine that can induce cytotoxic activity of CTL and NK cells and promote their secretion of IFN-gamma, TNF-\(\alpha\), GM-CSF, and other cytokines [51]. TNF-\(\alpha\) is the earliest and most important inflammatory mediator during the process of inflammation. It can activate neutrophils and lymphocytes, increase the permeability of vascular endothelial cells, regulate the metabolic activity of other tissues, and promote the synthesis and release of other cytokines [52]. These results showed that Shuidouchi reduced these proinflammatory expression levels and inhibited colitis. In this study, mice were used for all experiments. Because there are several differences between the mouse and human genome, and because the organs are different, the results of this study can confirm the effect of Shuidouchi on colitis only to a certain extent. Therefore, it is necessary to further verify the effect of Shuidouchi on the human body. At the same time, the mechanism of Shuidouchi in the human body also requires comprehensive and in-depth experiments. As basic research, this study has played a specific theoretical role.