Objective To investigate the role of macrophage?derived Act1 (nuclear factor kappa B activator 1) in the inflammatory bowel disease. Methods Genetically engineered mice carrying targeted suppression of Act1 in the mac?rophages (Anti?Act1) were used for the dextran sodium sulfate (DSS)?induced ulcerative colitis. The severity of colitis was assessed by weight loss, stool consistency, fecal blood index, colorectal length and H&E histology. The infiltration of CD45 + leukocytes and CD68 + macrophages in the inflammatory intestine was observed by immunohistochemical staining and expression levels of mRNA for inflammatory cytokines in colon tissues were analyzed by RT?qPCR. Results As com?pared with C57 mice, the anti?Act1 mice exhibited less severe acute colitis following DSS treatment, with reduced CD45 +leukocyte and CD68 + macrophage infiltrates in the colon tissue. Inflamed colons of the anti?Act1 mice expressed lower mR?NA levels of TNF?α, IL?1βand IL?6. Conclusions Targeted suppression of Act1 in the macrophages ameliorates dextran sodium sulfate?induced intestinal inflammation.

Objective To study the effect of heterozygous deficiency of SGT gene on the hematological and biochemical parameters of mice in young and elderly ages.Methods Blood samples were analyzed for complete hematological and biochemical parameters from heterozygous SGT-deficient and wild-type mice of 10-weeks and 6-months old mice, respectively.Results Age-related changes in most indexes were found statistically significantly different between young and elderly mice with the same genotype.Compared with the wild type at the same age, the platelet large cell ratio (P-LCR) was lower in young heterozygous SGT-deficient mice.However, platelet count, plateletcrit (PCT) and neutrophil count were more significantly lower in elderly heterozygous SGT-deficient mice (P<0.05).There was no significant difference for biochemical parameters ALT, AST, LDH, urea nitrogen, creatinine and blood glucose.Total and unconjugated bilirubin as well as ALP were significantly higher in elderly heterozygous SGT-deficient mice but not for conjugated bilirubin (P<0.05).In addition, significant differences existed for the lipids between two elderly groups (P<0.05).Conclusions Heterozygous deficiency of SGT gene induced changes of some hematological and biochemical parameters in elderly mice.It provides helpful information for further investigation on SGT involvement in some biological and pathological processes.

Objective To explore the effect of oridonin on the endoplasmic reticulum stress (ERS) in colonic epithelium of ulcerative colitis (UC) mice.Methods The UC mice model was established by sodium dextran sulfate (DSS),and the intervention group of oridonin and sulfasalazine was set up,the disease activity index (DAD was measured,the colonic tissue was evaluated by histopathologidscore (HPS),and RT-qPCR was used to detect the expression of inflammatory cytokines tumor factor-α (TNF-α),interleukin 6 (IL-6),cyclooxygenase 2 (COX-2),glucose-regulated protein 78 (GRP78),transcription factor EBP homologous protein (CHOP),activator transcription factor 6 (ATF6),protein kinase R like endoplasmic reticulum kinase (PERK) and inositol requiring enzyme 1α (IRE1α).Results The expression of TNF-α,IL-6,COX-2,GRP78,ATF6,CHOP,PERK and IRE1α mRNA in the colonic epithelium of the model group were all up-regulated obviously as compared with the healthy control group(P＜0.05,P＜0.01).When compared with the model group,DAI and HPS in oridonin-treated group were significantly decreased (P＜0.05,P＜0.01),which the curative effect was similar to that of the sulfasalazine group(P＞0.05,P＜0.01).The expression of TNF-α,IL-6,COX-2,GRP78,CHOP,ATF6 and PERK mRNA levels were significantly reduced in oridonin-treated group(P＜ 0.05,P＜0.01).Conclusion Oridonin can alleviate colonic inflammation induced by DSS and its mechanism may be related to ERS of colonic epithelial tissue.