Astilbin alleviates sepsis-induced acute lung injury by inhibiting the expression of macrophage inhibitory factor in rats.

Sepsis is a systemic inflammatory response syndrome caused by severe infections. Astilbin is a dihydroflavonol derivative found in many medicinal and food plants with multiple pharmacological functions. To investigate the effects of astilbin on sepsis-induced acute lung injury (ALI), cecal ligation and puncture was performed on rats to establish a sepsis-induced ALI model; these rats were then treated with astilbin at different concentrations. Lung injury scores, including lung wet/dry ratio, protein leakage, myeloperoxidase activity, and inflammatory cell infiltration were determined to evaluate the effects of astilbin on sepsis-induced ALI. We found that astilbin treatment significantly attenuates sepsis-induced lung injury and improves survival rate, lung injury scores, lung wet/dry ratio, protein leakage, myeloperoxidase activity, and inflammatory cell infiltration. Astilbin treatment also dramatically decreased the production of inflammatory cytokines and chemokines in bronchoalveolar lavage fluid. Further, astilbin treatment inhibited the expression and production of macrophage inhibitory factor (MIF), which inhibits the inflammatory response. Collectively, these data suggest that astilbin has a protective effect against sepsis-induced ALI by inhibiting MIF-mediated inflammatory responses. This study provides a molecular basis for astilbin as a new medical treatment for sepsis-induced ALI.

Modified shock index and mortality rate of emergency patients.

BACKGROUND: This study aimed to determine whether modified shock index (MSI) is associated with mortality that is superior to heart rate, blood pressure, or the shock index (SI) in emergency patients. METHODS: A retrospective database review was performed on 22 161 patients who presented to Peking Union Medical College Hospital Emergency Department and received intravenous fluids from January 1 to December 31, 2009. We gathered data of the patients on age, gender, vital signs, levels of consciousness, presenting complaints, and SI and MSI were calculated for all patients. RESULTS: Multivariate regression analysis was performed to determine the correlation between risk factors and outcome. There is a significant correlation between emergency patient mortality rate and patient's vital signs obtained at the triage desk (HR>120 beats/min, systolic BP<90 mmHg, diastolic BP<60 mmHg). MSI is a stronger predictor of emergency patient mortality compared to heart rate and blood pressure alone, whereas SI does not have a significant correlation with emergency patient mortality rate. CONCLUSION: MSI is a clinically significant predictor of mortality in emergency patients. It may be better than using heart rate and blood pressure alone. SI is not significantly correlated with the mortality rate of the emergency patient.

Role of corticotrophin releasing hormone in cerebral infarction-related gastrointestinal barrier dysfunction.

BACKGROUND: Corticotrophin releasing hormone (CRH) is believed to mediate stress-induced behaviors, implying a broader, integrative role for the hormone in the psychological stress response, and studies on CRH in physical stress are few. This study was undertaken to investigate whether CRH plays an important role in cerebral infarction-related gastrointestinal barrier dysfunction. METHODS: Thirty male Wistar rats were randomly divided into a pseudo-operation group (group C, n=10), a cerebral infarction group (group I, n=10), and a cerebral infarction + ic α-helical-CRH (9-41) group (group Aic, n=10). Urine samples were collected to determine the levels of epinephrine, norepinephrine, cortisol, and sucrose. At 24 hours after establishment of the models, blood samples were taken to determine the activity of diamine oxidase (DAO) and the concentration of D-lactic acid (D-lac). The stomach was taken to determine gastric Guth score, and the hypothalamus was also taken to determine tissue CRH protein expression using Western blotting. RESULTS: The hypothalamus CRH protein, the indicators of stress, the plasma DAO activity and plasma D-lac, urine sucrose exertion and gastric Guth score in group I were higher than those in groups Aic and C. CONCLUSIONS: After cerebral infarction, CRH in the hypothalamus was increased, the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system were activated, gastrointestinal permeability was increased, and gastrointestinal barrier function was destroyed. CRH receptor antagonist alleviated the gastrointestinal barrier function.

[Apoptosis of gastric mucosa and gastric barrier dysfunction in acute ischemic stroke].

OBJECTIVE: To evaluate the role of gastric mucosa apoptosis in the stress of ischemic stroke, and to discuss the relationship between gastric mucosa apoptosis and gastric barrier. METHODS: Ten dogs were artificially made ischemic stroke by operation (IS group), and another 10 shamly-operated dogs were served as control group. Sucrose permeability were measured after the operation. All dogs were sacrificed 24 hours after operation to measure the gastric mucosal apoptosis index, gastric gross classification, and histological score. RESULTS: The gastric mucosal apoptosis index in the IS group were significantly higher than in the control group (14.83 +/- 4.41 vs. 5.60 +/- 2.61, P < 0.05). The gastric mucosal apoptosis index were correlated with the sucrose permeability (r = 0. 89, P < 0.05) , gastric gross classification (r = 0. 87, P < 0.05), and histological score (r = 0.92, P < 0.05). CONCLUSIONS: Although ischemic stroke will not cause the obvious damage in the respiratory and circulatory system, it is responsible for the apoptosis of epithelial cell in the gastric mucosa and gastric barrier dysfunction. The apoptosis index is closely correlated with the damage of the function and morphology of the gastric barrier, indicating that the epithelial cell apoptosis acceleration in the gastric mucosa may result in the damage of gastric barrier function.