CBP can not only improve the general conditions but also effectively improve gut barrier dysfunction. The beneficial effect of CBP on gut barrier dysfunction is associated with the improvement of cytoskeletal instability, by downregulating iNOS through the removal of excess proinflammatory factors.

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Background: Prolyl endopeptidase (PREP) is a serine endopeptidase that regulates inflammatory responses. PREP inhibitors can reduce hepatocyte lipid accumulation and may participate in the progression of nonalcoholic fatty liver disease (NAFLD). We investigated whether disruption of PREP regulates hepatic steatosis and inflammation in mice with NAFLD.Methods: Wild-type and PREP gene disrupted mice were randomly divided into low-fat diet wild-type (LFD-WT), high-fat diet wild-type (HFD-WT), low-fat diet PREP disruption (LFD-PREP gt ), and highfat diet PREP disruption (HFD-PREP gt ) groups. Animals were euthanized at the endpoint of 32 weeks. The NAFLD activity score and number of inflammatory cells were determined by hematoxylin-eosin staining and immunohistochemical staining of liver tissue. The expression levels of inflammation-and lipid metabolismassociated genes in the liver and serum were detected by quantitative reverse transcription PCR, mass spectrometry, or enzyme-linked immunosorbent assay. Results:The body weight and epididymal fat tissue index of the HFD-PREP gt mice were significantly decreased compared with that of the HFD-WT mice. Moreover, the NAFLD activity score and liver function were attenuated in the HFD-PREP gt mice. Fat accumulation and the level of expression of mRNAs associated with lipid metabolism and proinflammatory responses were improved in the HFD-PREP gt mice.The number of CD68-positive cells in liver tissue and the serum levels of inflammation-associated factors were significantly decreased in the HFD-PREP gt mice compared with those in the HFD-WT mice. Further mechanistic investigations indicated that the protective effect of PREP disruption on liver inflammation was associated with the suppressed production of matrix metalloproteinases (MMPs) and proline-glycine-proline (PGP) and the inhibition of neutrophil infiltration.Conclusions: Loss of PREP lowers the severity of hepatic steatosis and inflammatory responses in a highfat diet-induced nonalcoholic steatohepatitis model. PREP inhibition may protect against NAFLD.

Objective. To observe effects of the thermal stimulation by moxibustion at different temperatures on cardiac function in brachycardia rat model and on mast cells in the local site of moxibustion at the Ximen Acupoint and to compare the differences of the effects of moxibustion at different temperatures. Method. Establish the brachycardia rat model with propranolol and observe effects of the thermal stimulation by moxibustion at different temperatures (38°C and 46°C). Results. The thermal stimulation by moxibustion at 2 temperatures may increase HR, MAP, LVSP, and +dp/dtmax and reduce t-dp/dtmax in brachycardia rats; the 46°C moxibustion group shows greater regulating effects on cardiac function in rats than that in the 38°C moxibustion group (P < 0.05). The thermal stimulation by moxibustion at 2 temperatures may promote degranulation of mast cells in the local site of moxibustion at the Ximen Acupoint; the degranulation rate in the 46°C moxibustion group is higher than that in the 38°C moxibustion group (P < 0.05). Conclusion. There is a certain association between the effect on the target organ and the effect in the local site of moxibustion. The moxibustion effect possibly resulted from local mast cells degranulation and different thermoreceptors activated by the thermal stimulation at different temperatures.

Breakdown of gut barrier function is present in patients with MODS and may be correlated with poor outcomes in the disease. CBP can not only improve the general conditions, as measured by the APACHE II score, but also improve gut barrier dysfunction by attenuating the breakdown and reorganization of occludin and ZO-1. This beneficial effect of CBP on gut barrier dysfunction is associated with down-regulation of iNOS.