Ulcerative colitis (UC) is a slowly developing, non-specific inflammatory bowel disease, characterized by abdominal pain, diarrhea, mucous bloody stools, or symptoms such as weight loss, urgency, and vomiting. It mainly invades the colon mucosa, destroys the mucosa and forms ulcers, often starting from the left colon and can develop from the proximal colon to the entire colon. The etiology and pathogenesis of UC are currently unclear. With the development of various disciplines and their mutual infiltration in recent years, people’s understanding of UC is also constantly deepening. Research has shown that the occurrence of UC is closely related to the imbalance of inflammatory factors and abnormal immune responses in patients’ intestines. The activation of inflammatory signals leads to an imbalance in the secretion of pro-inflammatory and anti-inflammatory cytokines, excessive accumulation of reactive oxygen species, and further accelerates the development of inflammation. Nuclear transcription factor (NF – κ B) and signal transduction and transcriptional activation factor 3 (STAT3) play important roles in mediating this abnormal immune response. The excessive secretion of various pro-inflammatory factors such as tumor necrosis factor – α (TNF – α), interleukin-6 (IL-6), interleukin-8 (IL-8), as well as the reduced release of anti-inflammatory factors such as interleukin-4 (IL-4) and interleukin-10 (IL-10), lead to intestinal inflammation in UC patients. Therefore, clinical treatment of UC can be achieved by inhibiting the release of pro-inflammatory factors and promoting the secretion of anti-inflammatory factors.

Cinnamaldehyde (CA), also known as cinnamaldehyde, cinnamaldehyde, or cinnamaldehyde, is an organic compound of the aldehyde class extracted from cinnamon trees and is the main component of its volatile oil. A large number of pharmacological studies on CA both domestically and internationally have shown that it has various pharmacological activities such as anti-inflammatory, anti ulcer, antipyretic and analgesic, anti-tumor, antibacterial, hypoglycemic, anti obesity, hypotensive, and antidepressant. The research team conducted preliminary studies on the therapeutic effect of purslane cinnamon on UC and found that the combination of the two can significantly improve the health activity status of UC mice, and is closely related to the improvement of intestinal microbiota balance. According to reports, CA can inhibit the expression of pro-inflammatory cytokines in macrophages, including TNF – α, IL-1 β, and nitric oxide (NO). There are also literature studies that suggest CA can improve DSS induced colitis by inhibiting the activation of NLRP3 inflammasome and the levels of miR-21 and miR-155 in the colon and macrophages. Therefore, our research group is investigating the therapeutic effect of CA on UC.

In this experiment, sulfasalazine (300 mg/kg) was used as a positive control, and CA was administered orally to UC mice induced by 3% sodium gluconate (DSS) at doses of 150, 250, and 500 mg/kg, respectively. Observe the changes in the state of mice before and after administration and perform DAI scoring. Use HE staining to observe the changes in the morphology of mouse colon tissue and perform pathological evaluation; ELISA kit and Western blot technology were used to detect the changes in the expression levels of inflammatory factors in mouse serum and inflammation related proteins in mouse colon epithelium.

Ulcerative colitis (UC) is common in developed countries in Europe and the United States with better economic and living standards, and its incidence rate is far higher than that in Asian countries. However, in recent years, with the economic development and improvement of living standards in Asian countries, the incidence rate of UC has increased year by year in China. The pathogenesis of UC is still unclear. It is known that imbalanced gut microbiota and disrupted internal environment will stimulate the intestinal mucosal immune system, alter mucosal permeability, and induce immune responses, leading to the occurrence of UC.

Cinnamaldehyde (CA) is an effective anti-inflammatory and antibacterial drug that can regulate and stabilize the gut microbiota, helping to improve intestinal barrier function. Our research group found in the preliminary study of purslane cinnamon that the combination of the two has a significant effect on UC in mice. In order to further clarify the main components of cinnamon in ulcerative colitis, this study established a DSS induced UC mouse model, administered CA treatment, and evaluated the therapeutic effect of CA. The DAI score results showed that CA can improve symptoms such as weight loss, diarrhea, and bloody stools in mice; The pathological scoring results showed that CA can protect the intestinal mucosa, reduce crypt cell damage and inflammatory cell infiltration, alleviate glandular disorder and disappearance, and improve inflammation. The occurrence of ulcerative colitis is closely related to the imbalance of inflammatory factors and abnormal immune response. UC patients have elevated levels of pro-inflammatory cytokines and decreased levels of anti-inflammatory cytokines in the colon, leading to immune dysfunction and the development of UC. In this study, CA significantly reduced the levels of pro-inflammatory cytokines IL-6, IL-8, and TNF – α in colon tissue (P<0.01), which may be related to the inhibition of STAT3 signaling pathway expression. At the same time, CA also significantly increased the levels of anti-inflammatory cytokines IL-4 and IL-10 in mouse colon tissue (P<0.01). There are many factors that affect the expression changes of inflammatory factors. Due to individual differences in animals and other factors, our experimental results did not show a dose-dependent relationship, while pathological scores showed a dose-dependent relationship. This is because inflammatory factors are micro indicators, and pathological scores display the overall situation of the intestinal tract. Therefore, the efficacy of drugs should be mainly judged based on animal disease activity index and pathological scores.

Pro-inflammatory cytokines are regulated by a complex network of intracellular signaling molecules, and nuclear transcription factor (NF – κ B) and signal transduction and transcription activator 3 (STAT3) play important roles in mediating this abnormal immune response. NF – κ B has obvious pro-inflammatory properties. Western blot technology was used to display the expression bands of NF – κ B protein. It can be seen that the expression of NF – κ B protein in the cytoplasm of the CA group was significantly higher than that of the model group, and there was a significant difference (P<0.01); From the band expression and grayscale values of p-STAT3 and STAT3 protein, it can be observed that the CA group showed a significant decrease in p-STAT3/STAT3 protein expression compared to the model group, with a significant difference (P<0.01). The above experimental results indicate that the protective effect of CA on DSS induced UC mice is closely related to the activation of inflammatory key proteins NF – κ B and STAT3.

In summary, CA can significantly improve weight loss, decreased colitis disease score, and inflammatory changes in colon tissue caused by enteritis. It reduces the secretion of pro-inflammatory factors TNF – α, IL-6, and IL-8, promotes the expression of anti-inflammatory factors IL-4 and IL-10, and its anti-inflammatory effect may be related to the inhibition of the immune inflammatory signaling pathways of NF – κ B and STAT3. This experiment only studied its efficacy at the animal level. In the future, we will investigate its therapeutic mechanisms at the cellular, molecular, and genetic levels to provide more options for the treatment of UC in China.