Kearneygrau6338

protective effect, which can significantly improve liver necrosis condition and inhibit inflammation. Therefore, adequate vitamin D can retain liver physiological balance to resist liver injury.Objective To investigate the effect of R2* value on the evaluation of different degrees of hepatic warm ischemia-reperfusion injury (WIRI) and liver regeneration after partial hepatectomy in rabbits. Methods Thirty healthy adult male New Zealand White rabbits were randomly divided into five groups. Hepatic caudal lobectomy was performed in both the control and the warm ischemia time-dependent variation group. After reperfusion, routine MRI and BOLD MRI scans were performed for each group at 6 h, 3 d, 7 d, 14 d and 30 d, respectively, and then R2* value and liver regeneration rate (LRR) were measured and calculated. After 30 days of scanning, the serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), myeloperoxidase (MPO), tumor necrosis factor - α (TNF - α), interleukin-6 (IL-6) and proliferating cell nuclear antigen (PCNA) were detected in frozen rabbit liver tissues, and the pathological sections were collected. Repeated measures analysis of variance was used to evaluate the changes of R2* value, LRR and its influencing factors at different follow-up time and warm ischemia time in each group. Pearson's or Spearman's correlation analysis was used to evaluate the correlation of R2* value with LRR and various biochemical indexes. Results The interaction between different follow-up time and warm ischemia time (F = 24.600, P 0.05). Conclusion The R2* value may be used for noninvasive and quantitative evaluation of microstructural changes of WIRI and affect liver regeneration after partial hepatectomy in rabbits. A certain degree of WIRI (≤30 min) after partial hepatectomy can promote liver regeneration in rabbits. Furthermore, as the warm ischemia time prolongs, the promoting effect becomes more pronounced, and if the warm ischemic time exceeds 30 minutes, the promoting effect is significantly reduced.Objective To preliminary explore the changes in blood system in pyrrolizidine alkaloids (PAs)-related liver damage. Methods General situation, liver function, biochemical blood test, routine blood test, coagulation function markers, etc., of 77 cases with drug-induced liver damage admitted to the Zhongshan Hospital Affiliated to Fudan University from 2012 to 2019 were retrospectively analyzed. Patients' were divided into PA group, other traditional Chinese medicine group and Western medicine group according to their medication history. Simultaneously, the changes in liver function were observed in the established mice model of monocrotaline-induced liver damage. Liver tissues HE staining and blood routine indexes were observed. Results 24 cases received PA, 24 cases received other traditional Chinese medicine, and 29 cases received western medicine. Alanine aminotransferase was lower in PA group than the other two groups (P less then 0.05), and the total bilirubin and direct bilirubin were significantly low Conclusion PA-related liver damage has lower peripheral platelet counts, and the peripheral platelet counts of these patients are lower than other types of drug-induced liver damage. In addition, increased D-dimer in patients with PA-related liver damage indicate a potential risk of thrombosis.Objective To investigate the expressional condition of interleukin-16 (IL-16) in the liver and serum of patients with primary biliary cholangitis (PBC). Methods Liver biopsies samples were collected from 70 cases and 10 healthy controls, and serum samples were collected from 62 cases and 87 healthy controls. The expression of IL-16 in liver was detected by immunohistochemistry, and the serum level of IL-16 was determined by enzyme-linked immunosorbent assay. The correlation between the expression level of IL-16 and the severity of disease was determined by correlation analysis with clinical biomarker. The t-test was used for normally distributed data. Wilcoxon signed rank sum test was used for non-normally distributed data. Results The expression level of IL-16 in the liver of PBC patients was significantly higher than that in the healthy control group (P = 0.002 5), and it was mainly expressed in infiltrating lymphocytes in the portal area. Correlation analysis showed that the level of IL-16 in liver tissue was positively correlated with the degree of liver inflammation (r = 0.36, P = 0.002). In addition, the serum IL-16 level of PBC patients were significantly higher than that of healthy people (P = 0.000 5), and serum IL-16 level was correlated with the level of cholestasis biomarker γ-glutamyltransferase (r = 0.31, P = 0.03). Conclusion The expression level of IL-16 is significantly increased in liver and serum of PBC patients, and it is positively correlated with the severity of the disease, suggesting that IL-16 may be used as a biomarker to assess the severity of the disease.The key factors driving the pathogenesis of alcoholic liver disease are still not fully understood. At present, it is believed that the direct toxic effects of ethanol and its intermediate metabolite acetaldehyde can cause oxidative stress, mitochondrial damage, adipogenesis, malnutrition, intestinal endotoxin leakage, etc., thereby participating in the occurrence and progression of alcoholic liver disease. Among the many pathogenic factors that have been revealed, the immunological mechanism plays an important role. Therefore, the role of immune cells and inflammatory mediators has attracted much attention. This article reviews and summarizes the new progress of specific immune cell mechanisms involved in innate and adaptive immune response during the formation and development of alcoholic liver disease, and proposes potential therapeutic targets and clinical trials of related new drugs, which may improve the re-recognition of molecular mechanism and treatment expectation in clinical practice.Nonalcoholic fatty liver disease (NAFLD) has become the most common chronic liver disease in the world. Liver cirrhosis, liver cancer and a variety of extrahepatic chronic diseases are important risk factors for NAFLD. Currently, there is still a lack of effective therapeutic drugs. Liver inflammation is a key driving factor for the progression of NAFLD, so regulating liver inflammation may provide a potential means to delay and reverse the progression of nonalcoholic steatohepatitis (NASH). Studies have found that the gut-liver-immune axis plays an important role in the progression of NASH. Gut microbiota can use its metabolites to induce glycolipid toxicity, oxidative stress and intestinal barrier damage, while bacterial components such as lipopolysaccharides, peptidoglycans, bacterial DNA and extracellular vesicles can translocate into the liver through the damaged intestinal barrier, causing excessive activation of immune cells, thus aggravating liver inflammation and promoting the progress of NASH. selleck chemicals This paper focuses on the gut-liver-immune axis to analyze the gut microbiota mediated liver immunity and its mechanism in the occurrence and development of NASH, so as to lay a theoretical foundation for the research and development of new therapeutic strategies for NASH.