## 4 Discussion
The DAI index is an important index for the observation of colitis in mice. With aggravated inflammation, the DAI increases, and the DAI index decreases after the remission of colitis [28]. Consequently, colitis in mice could be relieved using Shuidouchi extract from Shuidouchi that was fermented with the improved process. Studies have shown that the contractile effect of endothelin on blood vessels can lead to colonic mucosal erosion, which can result in ulcers in severe cases that aggravate colitis [29]. SS inhibits gastric acid secretion and suppresses gastrointestinal inflammation. Deficiency in SS can promote a large amount of gastrointestinal fluid secretion and aggravate colitis [30]. SP regulates the nervous and immune systems of the body, and the accumulation of substance P in the body leads to an aggravation of colitis [31]. Excessive SP can directly result in colitis and it can inhibit colitis in antagonistic antibodies [32]. VIP can regulate the iNOS transcription in vivo, inhibiting the conversion of excessive iNOS to NO in colonic tissues and avoid intestinal mucosal damage that is caused by large amounts of NO. VIP can also inhibit disorders of the immune system that are caused by colitis [33]. Therefore, Shuidouchi fermented using this improved technique can protect the colon and prevent colitis by regulating the ET, SS, SP, and VIP. IL-2 is a cytokine secreted by Th2 cells, which are directly related to colitis. Th2 cells can mediate the immune response to exert an effect on colitis. IL-2 can inhibit colitis by influencing Th2 cells [34]. IL-10 is a cytokine that is secreted by Treg cells, which exert an immunosuppressive effect to aggravate colitis [35]. The obtained results indicate that Shuidouchi that was fermented with this improved process can inhibit colitis by regulating the cytokines IL-2 and IL-10. After the onset of colitis, the original aggregated neutrophils in the colon disperse, and the influx of neutrophils into the tissues markedly increases the MPO level [36]. After inflammation, free radicals, such as ROS and RNS, accumulate rapidly in vivo; consequently, the damage and toxicity of the colon tissue are further aggravated, and the degree of colitis is considerably increased [37]. Studies have shown that the GSH and SOD levels in colonic tissues decreased in response to colitis, whereas MDA, a peroxide product, increased significantly [38]. In the current study, the improved Shuidouchi process significantly influenced the MPO, SOD, GSH, and MDA levels in mice with colitis and can thus prevent colitis. The antioxidant capacity of Shuidouchi is directly reflected in the impact on the above indexes in vivo; therefore, the effects of Shuidouchi on colitis are directly related to its antioxidant effect. The results showed that nNOS could regulate the concentration of NO in tissues and protect tissues from damage that is caused by excessive NO. Simultaneously, nNOS can control iNOS and avoid iNOS overexpression, thus resulting in an aggravation of inflammation [39]. eNOS can regulate the NO level in the body, thus maintaining the balance of NO in the body and the normal state of the colon tissues, which can regulate colon tissue injury and colitis [40]. NO is produced by two cNOS subtypes that are associated with iNOS, accelerating nitrification and oxidative damage, while also increasing inflammatory factors [41]. A high amount of iNOS can convert an equally high amount of NO, and excessive NO can lead to colonic tissue damage, resulting in the aggravation of colitis [40]. Studies have also shown that the expression pattern of iNOS is related to inflammation, and the inhibition of iNOS can reduce inflammation [41]. Simultaneously, inflammatory bowel disease (IBD) is associated with the excessive production of NO by iNOS, and the amount of NO in the intestinal tract and saliva of patients with IBD is increased when compared to control subjects [42]. Animal experiments have also shown that the inhibition of iNOS attenuated the DSS-induced colitis in mice [43].