Liver Metabolomics Reveals the Effect of Lactobacillus reuteri on Alcoholic Liver Disease.

Alcoholic liver disease (ALD), a type of chronic liver disease that is prevalent worldwide, is still identified to have a poor prognosis despite many medical treatment protocols. Thus, it is urgent to develop and test new treatment protocols for ALD. Lactobacillus reuteri (L. reuteri) has been widely used in the clinical treatment of digestive system diseases, but studies on the protective effect of L. reuteri on ALD are considered to be rare. Therefore, in the present study, we examined the effect of L. reuteri on ALD and provide data that are significant in the development of new treatment protocols for ALD. An ALD model has been established in C57BL/6J mice treated according to the Gao-binge modeling method. Mice in the treatment group were administered with L. reuteri. Hematoxylin and eosin (H&E) staining, oil red O staining, immunohistochemistry, and biochemical analyses were performed to detect the phenotypic changes in the liver among mice in the different treatment groups. L. reuteri treatment reversed inflammatory cell infiltration and lipid accumulation. Moreover, AST, ALT, TG, and TCH levels were also reduced in the probiotics-treatment group. Five candidate biomarkers were found in the liver metabolites of different treatment groups by UPLC/QTOF-MS and a multivariate analysis. Several fatty acid metabolic pathways such as linoleic acid metabolism and glycerolipid metabolism were involved. All these findings suggested that L. reuteri treatment reversed the phenotype of ethanol-induced hepatitis and metabolic disorders. These findings provide evidence that L. reuteri might serve as a new therapeutic strategy for ALD.

Bronchogenic cyst of the stomach: A case report and literature review.

Bronchogenic cyst (BC) is a rare congenital disease with pre-embryonic intestinal malformation. BC of the stomach is rare. The present study reported on the case of a 68-year-old male who presented with a spleen and stomach space mass detected incidentally upon a routine health examination. The patient underwent laparotomy. Postoperative histopathological diagnosis confirmed BC of the stomach. Postoperative recovery was smooth and the patient is currently under follow-up. A literature review suggested that BC is a rare disease and the location of the stomach is very rare. Indications of surgical intervention remain controversial for asymptomatic cases. Owing to no specific clinical or radiologic features to define the disease profile for diagnosis, surgery may be a good choice for both diagnosis and therapy if the patient's condition permits.

Kaempferol from Penthorum chinense Pursh suppresses HMGB1/TLR4/NF-κB signaling and NLRP3 inflammasome activation in acetaminophen-induced hepatotoxicity.

Acetaminophen (APAP) is one of the safest and most effective over-the-counter (OTC) analgesics and antipyretics, but excessive doses of APAP will induce hepatotoxicity with high morbidity and mortality worldwide. Kaempferol (KA), a flavonoid compound derived from the medicinal and edible plant of Penthorum chinense Pursh, has been reported to exert a profound anti-inflammatory and antioxidant activity. In this study, we explored the protective effect and novel mechanism of KA against APAP-induced hepatotoxicity. The results revealed that KA pretreatment significantly reduced the levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT), relieved hepatocellular damage and apoptosis, attenuated the exhaustion of glutathione (GSH) and accumulation of malondialdehyde (MDA), increased the expression of antioxidative enzymes (e.g., heme oxygenase 1 (HO-1) and NADPH quinone oxidoreductase 1 (NQO1)), and thus restrained APAP-induced oxidative damage in the liver. KA suppressed the expression of NLRP3 and reduced the levels of pro-inflammatory factors, including interleukin-1 beta (IL-1ß), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6). Moreover, KA remarkably inhibited high-mobility group box 1 (HMGB1) and toll-like receptor 4 (TLR4) expression as well as nuclear factor kappa-B (NF-κB) activation for liver protection against APAP-induced inflammatory responses and apoptosis. Taken together, our findings suggested that KA could effectively protect hepatocytes from APAP hepatotoxicity through the up-regulation of HO-1 and NQO1 expression, the down-regulation of NLRP3 expression, and the inhibition of the HMGB1/TLR4/NF-κB signaling pathway.