Abstract:
A mouse model of ulcerative colitis was established through feeding C57BL/6 mice continuously 3% dextran sulfate sodium salt (DSS) for 7 days, to examine the anti-inflammatory effect of cocoa powder (CP) and its molecular mechanism. Twenty mice were randomly divided into four groups: control group (drinking water regularly), model group (3% DSS drinking water), and CP low and high dose treatment groups (50 and 100 mg/(kg•d) gavage plus 3% DSS drinking water). The results showed that compared with the control group, the model group lost more body weight, with its colon length (6.89 cm) significantly shorter than that of the control group (9.85 cm), and its histopathological score (5.20) significantly higher than that of the control group (0.60). In the meantime, the mRNA and protein expression levels of pro-inflammatory cytokines TNF-α, IL-6 and IL-1β in the intestinal tissues of mice increased by 9.72 times, 7.08 times, 7.39 times and 0.93 times, 0.44 times and 0.52 times, respectively, while the phosphorylation levels of a key protein of the NF-κB signaling pathway, p65, and IκBα protein increased by 4 times and 2.12 times, respectively, with the differences being statistically significant (p<0.01). Compared with the model group, the weight loss, colon length and histopathological score of the low-dose and high-dose CP-treated groups were significantly reduced, with the colon lengths and histopathological scores being 8.16 cm and 9.19 cm, and 3.20 and 2.00, respectively. The mRNA expression levels of pro-inflammatory cytokines TNF-α, IL-6 and IL-1β decreased by 0.64, 0.72 and 1.05 times, and 2.03, 2.27 and 2.07 times, respectively, the protein expression levels decreased by 0.22, 0.14 and 0.18 times, and 0.58, 0.37 and 0.68 times, respectively, and the phosphorylation levels of p65 and IκBα proteins decreased by 0.62 and 2.07 times, and 1.69 and 2.19 times, respectively. All the differences were statistically significant (p<0.05). In summary, CP exhibited a significant inhibitory effect against DSS-induced colitis in mice, and its molecular mechanism was related to the inhibition of NF-κB p65 signaling pathway activation.
