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Objective:To investigate the mechanism by which chronic psychological stress aggravates intestinal barrier damage and promotes the development of enteritis through inhibiting Wnt/β-catenin pathway, so as to provide a new therapeutic strategy for the clinical diagnosis and treatment of inflammatory bowel disease (IBD).Methods:A comorbidity model of chronic psychological stress and enteritis was established using C57BL/6J mice. HE staining was used to analyze the effects of chronic psychological stress on the intestinal pathological damage in mice with enteritis. ELISA was used to detect the expression of proinflammatory cytokines. The ultrastructural changes of colonic cells and the state of intestinal mucus layer were observed under transmission electron microscope and scanning electron microscope. The secretion of mucoprotein 2 (MUC2) and the expression of cell proliferation marker Ki67 were detected by immunofluo rescence staining. The numbers of goblet cells were detected by Alcian blue-periodic acid-Schiff (AB-PAS) staining. Western blot was performed to analyze the expression of tight junction protein between intestinal epithelial cells, β-catenin which was a key protein of Wnt/β-catenin pathway maintaining crypt proliferation, and downstream protein c-myc.Results:The sugar water consumption ratio decreased, but tail suspension immobility time, the swimming immobility time and the expression of corticotropin releasing hormone (CRH) in hypothalamus increased (all P<0.05) in the stress group as compared with those in the control group. Chronic psychological stress promoted weight loss and colonic shortening in mice with enteritis, exacerbated pathological damage and enhanced the release of pro-inflammatory factors. Moreover, increased disappearance of intestinal epithelial microvilli and severe cellular ultrastructural damage were also observed in the stress+ dextran sulfate sodium salt (DSS) group. There was no pathological damage in the control and stress groups. Chronic psychological stress aggravated intestinal barrier injury and inhibited intestinal barrier repair by inhibiting Wnt/β-catenin pathway. Conclusions:In the mouse model of DSS-induced enteritis, chronic psychological stress preconditioning inhibited the Wnt/β-catenin pathway, weakened the repair ability of intestinal epithelium, aggravated the loss of mucus layer of intestinal barrier and the damage of tight junction structure, and promoted the development of enteritis. In the absence of enteritis, chronic psychological stress had no significant effects on the Wnt/β-catenin pathway and the intestinal barrier.
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Psychological stress （pressure） has gradually become an important factor affecting human physical and mental health， and is one of the important factors in the progression of clinical chronic refractory diseases. Psychological stress response can be attributed to the category of emotional illness in traditional Chinese medicine （TCM）. In the theory of TCM， the liver controls dispersion and regulates mental activity. Relevant scholars believe that the liver is the core of psychological stress response in the TCM theory. When being stimulated by chronic or repeated psychological stress， the body can gradually change from the initial depression and anxiety-rela behaviors to the gastrointestinal dysfunctions， which is similar to the formation process of the syndrome of liver depression and spleen deficiency with liver-spleen disharmony. The syndrome of liver depression and spleen deficiency is also the common syndrome of TCM for psychological stress-related diseases. With the effect in soothing liver and invigorating spleen， Xiaoyaosan has been regarded as the classic formula for anti-stress. Modern studies have showed that gut microbiota not only get involved in the movement， structure and function of the digestive tract， but also affect the brain function and behavior of the host through the gut-brain axis. Therefore， the microbiota-gut-brain axis has become an important part of psychological stress to trigger the body's gastrointestinal symptoms and abnormal brain behaviors. Focusing on psychological stress， the authors explored the correlation between the syndrome of liver stagnation and spleen deficiency and the microbiota-gut-brain axis， and the intervention mechanism of Xiaoyaosan， so as to enrich the scientific connotation of the syndrome of liver stagnation and spleen deficiency.
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With the rapid development of our country,people are facing more and more psychological problems.It has been demonstrated that persistent stress and depression,which leads to continuously elevated levels of stress hormones,might eventually compromise host defenses against bacterial or viral infection while increasing the reoccurance of autoimmunity and the incidence of malignancy/metastasis.Even though the molecular mechanisms by which chronic psychological stress inhibits the effector subsets in the immune system have been partially disclosed,it remains elusive whether chronic psychological stress also affects the regulatory subsets and if yes,what are the underlying mechanisms.Here,we review the findings in this field.
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【Objective】To observe the effect of Modified Sini Powder(MSP)on the expression of hippocampal neuronal nitric oxide synthase(nNOS)in rats with chronic psychological stress.【Methods】Twenty-four Wistar rats were randomized into 3 groups: normal group,model group(receiving random stress stimulation for 21 days),and MSP group(receiving gastric infusion of MSP 3.38 g for each rat one hour before stimulation).The normal group and the model group received the same volume of saline.The expression of hippocampal nNOS was detected with immunohistochemical method.【Results】nNOS expression was found in neuronal pyramidal cells of hippocampus CA3 area in the three groups.The expression was obvious,positive cell count and its scoring were increased in the model group as compared with the normal group(P
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Aim The purpose of this study was to investigate mec ha nism of different therapies and formulas regulating chronic psychological stress . Methods The way of chronic bandaging and confining activity space w as adopted to establish chronic psychological stress rat model. The effects of d ifferent therapies and formulas on CRH mRNA expression in Hypothalamus were anal yzed by RT-PCR method. Results There was significant increase of CRH mRNA expression in Hypothalamus of rats with continual 2 wk psychological stres s(P
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Objective: To observe the effect of chronic psychological stress on change of function of learning and memory, and CD4, and CD8 in mice. Methods: 50 BALB/c mice were randomly divided into control group and immobilization stress group (n=25 in each group). The mice mode of stress was made by restraint for 6 hours per day. Suspend tail test was performed on change of behaviors in mice. RIA was employed to measure levels of neuropeptide Y in the brain. Results: Compared with the control group, the mean escape latency of the mice in the chronic restraint groups was longer than that of the control mice (P