BackgroundInterleukin-22 (IL-22) is a member of the IL-10 family of anti-inflammatory cytokines that mediates epithelial immunity. IL-22 expression was found to be increased in patients with ulcerative colitis (UC). Whether genetic polymorphisms of IL-22 also influence UC risk is still unknown. The purpose of this study was to investigate the association between the IL-22 gene polymorphisms (−429 C/T, +1046 T/A and +1995 A/C) and the risk of UC in Chinese Han patients.MethodsThis hospital-based case–control study comprised 180 patients with UC and 180 age- and gender-matched controls. Genotypes of 3 common polymorphisms of the IL-22 gene were determined by fluorogenic 5′ exonuclease assays (TaqMan).ResultsPatients with UC had a significantly higher frequency of IL-22 −429 TT genotype [odds ratio (OR) =2.43, 95% confidence interval (CI) = 1.35, 4.37; P = 0.003] and −429 T allele (OR =1.54, 95% CI = 1.14, 2.07; P = 0.004) than controls. The findings are still emphatic by the Bonferroni correction. The IL-22 +1046 T/A and IL-22 +1995 A/C gene polymorphisms were not associated with a risk of UC. When stratifying by clinical type, location and disease severity of UC, no significant differences were found in any groups.ConclusionThis is the first study to provide evidence for an association of IL-22 −429 C/T gene polymorphisms with UC risk. Additional well-designed large studies were required for the validation of our results.Virtual SlidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/13000_2014_183
Background: Long Chai Fang (LCF) is a traditional Chinese medicine (TCM) formula for treating chronic hepatitis B (CHB) in clinical settings; however, its related mechanism remains unclear.Methods: To address this issue, network pharmacology and an integrative method that combines dotblot hybridization and metabolomics analysis were employed. Network pharmacology was performed to investigate the material basis and potential mechanisms of LCF against CHB. The effect of LCF on Duck hepatitis B virus (DHBV) replication was evaluated. The metabolomics analysis was conducted to identify potential biomarkers in duck serum. Results:The network pharmacology approach revealed 133 potential active components, 897 drug targets, 979 disease targets, and 185 drug-disease targets, while the Kyoto Encyclopedia of Genes and Genomes enrichment analysis identified 165 pathways. LCF significantly inhibited DHBV-deoxyribonucleic acid replication on day 10 and day 3 after the cessation of treatment. Notably, the low-dose LCF group showed the best inhibitory effect. The obviously sustained anti-DHBV activity of LCF inhibited viral replication, and a rebound reaction was found. Phosphatidylcholine and phosphatidylethanolamine classes, which are mainly involved in liver cell repair and energy metabolism through phospholipid metabolic pathways, were identified by metabolomics analysis.Conclusions: our results showed that the main active ingredients of LCF appear to be metacarpi, isorhamnetin, glypallichalcone, and phaseolinisoflavan. This study provides novel strategies for using a LCF formula against CHB in future research.
Background Jian Gan powder (JGP), a traditional Chinese medicine (TCM) formula, has shown a considerable protective and therapeutic effect on hepatitis virus-induced immunological liver injury (ILI) in the clinic. However, the underlying mechanisms of the protective effects of JGP on ILI remain unknown. Evidence suggests that TCM or TCM formula can affect the intestinal microbial community and metabolic function to control liver disease progression. Results JGP treatment reduced inflammatory cytokine expression and promoted liver cell proliferation. The fecal 16S rRNA gene sequencing and LC-MS-based metabolomics analysis revealed that JGP could notably shape the gut microbiota structure and modify metabolic profiles. JGP treatment could restore the dysbiosis of Alloprevotella, Burkholderia-Caballeronia-Paraburkholderia, Muribaculum, Streptococcus, and Stenotrophomonas. Moreover, fecal metabolite profiles reflecting microbial activities showed that JGP modulated the disorder of biotin metabolism and steroid hormone biosynthesis in ILI mice. What’s more, the metabolites, Allylestrenol, Eplerenone, PE (P-20:0/0:0), SM d27:1, Soyasapogenol C, Chrysin, and Soyasaponin I were notably changed and remarkably reversed after JGP treatment. Conclusion JGP exerts anti-inflammatory and pro-proliferative effects and restores the dysbiosis of the gut microbiota and metabolism of the immunological liver injury mice. These results provided a new perspective that intestinal microbiota and their metabolites might be potential targets for elucidating the mechanism of JGP on the improvement of ILI.
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