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Aim To investigate the role of metabolites of eicosapentaenoic acid (EPA) in promoting the transdifferentiation of pancreatic α cells to β cells. Methods Male C57BL/6J mice were injected intraperitoneally with 60 mg/kg streptozocin (STZ) for five consecutive days to establish a type 1 diabetes (T1DM) mouse model. After two weeks, they were randomly divided into model groups and 97% EPA diet intervention group, 75% fish oil (50% EPA +25% DHA) diet intervention group, and random blood glucose was detected every week; after the model expired, the regeneration of pancreatic β cells in mouse pancreas was observed by immunofluorescence staining. The islets of mice (obtained by crossing GCG
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Aim To investigate the effect of dietary intake of o)-3 poly unsaturated fatty acids ( u>-3 PUFAs) on the immune function of chronic graft versus host disease (cGVH) lupus model mice.Methods A single intraperitoneal injection of bml2 mice lymphocytes was used to establish a cGVH mouse model.On the day of modeling, 90% cd-3 PUFAs and 97% EPA were given by gavage for 14 days.The immune indexes of mice were evaluated by flow cytometry, and the serum total J J J ∗ IgG levels were measured by ELISA.Results Compared with control group, cGVH group significantly down-regulated Treg subsets, and up-regulated the Tfh , GC B and plasma subsets in the lupus mice.Comparer] with model control group, u>-3 PUFAs could significantly elevate Treg subsets, and decrease TFH, (X] B, and plasma subsets; serum total IgG levels in the 97% EPA group were significantly reduced.Conclusion In the cGVH lupus mouse model, co-3 PUFAs can suppress some immune functions by increasing Treg cells, reducing TFH, GC B, plasma cells and inhibiting the secretion of IgG.Such immunomodulatory effect provides new sights into the development of a potentially novel treatment modality for cGVH.
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Aim To investigate the effects of FKBP38 gene on nonalcoholic fatty liver disease ( NAFLD ) model induced by methionine and choline deficiency j J diet (MCD) in mice.Methods The mutant model of hepatocellular specific deletion of FKBP38 gene was successfully established.The mice were divided into wild-type group ( WT) and homologous knockout group (L-FKBP38 ).Mice were fed with MCD for four weeks to construct NAFLD model.Liver injury was e- valuated by the contents of alanine transaminase (ALT), aspartate transaminase (AST) in the serum samples.We also performed HE staining, examined lipid accumulation by triglyceride (TG) and total cholesterol (CHO) and oil red staining, as well as macrophage infiltration by F4/80 immunohistochemical stai-ning of the liver sections.Fatty acid metabolism-relat ed genes were quantifier] by Quantitative Real-time PCR assays.Results Comparer] with WT group, the levels of ALT, AST, TG and CHO in serum signifi- eantly inereased ( P < 0.05 ) ; liver damage , lipid ac- eumulation, and maerophage infiltration were markedly more severe, and the expressions of fatty aeirl oxidation related genes PPARa, ACOX-1 , CPT-la and SIRT3 markedly rleereaserl ( P < 0.05) in the liver samples of L-FKBP38 group.Conclusions Hepatocellular speeifie deletion of FKBP38 intensifies lipid accumula- tion by inhibiting fatty aeid oxidation in the liver, thus exaeerbating nonaleoholie fatty liver disease.