Shionone Relieves Ulcerative Colitis by Regulating the p38 MAPK/NF-κB Pathway

Ulcerative colitis is a serious intestinal disorder, which can lead to a variety of complications, and in severe cases, the risk of becoming cancerous, seriously harming human health. This study aimed to investigate the anti-inflammatory effect of shionone on ulcerative colitis and analyze its potential mechanism of action. Cell counting kit-8 and lactate dehydrogenase kits were used to detect the viability of colorectal adenocarcinoma Caco-2 cells and lactate dehydrogenase activity, respectively. Apoptosis of the treated cells was detected using flow cytometry. Western blot assay was performed to detect the expression levels of apoptosis-related proteins and p38 MAPK/NF-κB signaling pathway-related proteins. Changes in inflammatory factor secretion in cell supernatants were detected using enzyme-linked immunosorbent assay. Shionone showed no toxic effects on the cells. Shionone enhanced the proliferative activity of lipopolysaccharide-induced Caco-2 cells, decreased lactate dehydrogenase activity, and reduced apoptosis. It also suppressed the secretion of inflammatory factors. Shionone was found to affect the p38 mitogen-activated protein kinase (MAPK)/nuclear factor-kappa B (NF-κB) signaling pathway by decreasing the expression levels of p-p38 and p-p65 proteins and decreasing the ratio of p-p38/p38 and p-p65/p65. Moreover, the p38 mitogen-activated protein kinase agonist, P79350, significantly reversed the effects of shionone on lipopolysaccharide-induced Caco-2 cells, as demonstrated by the promotion of the expression of p-p38 and p-p65, the elevation of the p-p38/p38 and p-p65/p65 ratios, an increase in cell apoptosis, and an increase in inflammatory factor secretion. Shionone alleviated ulcerative colitis through the p38 MAPK/NF-κB signaling pathway, providing a novel therapeutic target for the management of ulcerative colitis.