Pan Chen,Hongliang Yao,Weiwei Su,Yudong He,Keling Cheng,Yonggang Wang,Wei Peng,Peibo Li
Aims Sleep deficiency has been reported to be associated with some oral health problems. Oral ulcers are very common lesions of the oral mucosa, which severely impact patients' quality of life. However, the association between sleep deficiency and the oral ulcer remains unknown. The present study aims to explore the effects of sleep deficiency on oral ulcers. Main methods Rats were divided into normal control group (n = 30) and oral ulcer group (OU group, n = 50). Model rats with phenol-induced oral ulcers were deprived of sleep for 72 h by using the modified multiple platform technique. Key findings Sleep deprivation worsened oral ulcers and delayed healing process in rats. In addition, sleep deprivation increased the γ-aminobutyric acid (GABA, P < 0.01) and 5-hydroxytryptamine (5-HT, P < 0.05) levels in serum and brain, the corticotrophin (ACTH, P < 0.05), corticosterone (CORT, P < 0.01), immunoglobulin (Ig)M ( P < 0.01), tumor necrosis factor-alpha (TNF-α) ( P < 0.01), interleukin (IL)-1β ( P < 0.01), IL-6 ( P < 0.01), IL-8 ( P < 0.01), monocyte chemoattractant protein-1 (MCP-1) ( P < 0.01), and 8-hydroxy-deoxyguanosine (8-OHdG, P < 0.01) levels in serum. Sleep deprivation also up-regulated malonaldehyde (MDA) ( P < 0.05), TNF-α ( P < 0.05), and IL-1β ( P < 0.01) levels in oral mucosa tissue and delayed superoxide dismutase (SOD, P < 0.05) activity recovery. Significance These data suggest that sleep deprivation impaired the oral ulcer healing in rat oral mucosa, and the mechanisms of this effect are probably related to neuro-immuno-endocrine system and oxidative stress.
Yue Su,Zhengying Cui,Xinyan Yang,Yujun Jiang,Wei Zhang,Yu Zhang,Chaoxin Man
Ulcerative colitis (UC) is an immune-mediated intestinal disease without a comprehensive cure, and the alleviation of UC has become an urgent problem. The results showed that JY062 with its EPS group (JEC) alleviated the intestinal barrier damage caused by LPS. After JEC intervention on Caco-2 cells, resulted in upregulation of ZO-1, Claudin-1, Occludin and MUC2 transcript levels and decreased mRNA expression of Claudin-2 (p < 0.05). JEC effectively attenuated the inflammatory response in UC mice and restoration of immunoglobulin levels (IgG, IgM and IgA), which resulted in shortening and swelling of the colon, disappearance of goblet cells, infiltration of inflammatory cells and mucosal damage were alleviated in mice. Similarly, changes in the expression of MUC2 and tight junction proteins after JEC intervention also occurred in UC mice. Administration of JEC significantly inhibited the differentiation of pro-inflammatory Th17 cells in the thymus and peripheral blood, promoted the differentiation of CD4+ T cells to Treg cells, and effectively regulated DSS-induced macrophage imbalance, which was manifested by the polarization of pro-inflammatory M1 macrophages to anti-inflammatory M2 macrophages. This study clearly demonstrates that JEC could significantly prevent intestinal barrier on DSS-induced experimental colitis and could be applied as a potential symbiotic strategy to assist in the alleviation of UC.
危险品化学品经营许可证（带存储）