期刊文献+
共找到3篇文章
< 1 >
每页显示 20 50 100
Therapeutic Effect and Mechanism of New Maixian Powder on DSS-induced UC Rats 被引量:1
1
作者 Minjun FU Rongzhen SHI +2 位作者 jianjun shen Meixia YANG Hongbin ZHENG 《Medicinal Plant》 CAS 2018年第3期58-61,共4页
[Objectives] To study the therapeutic effect and mechanism of New Maixian Powder on ulcerative colitis( UC) rats through observing its regulatory effect on the protein kinase R-like endoplasmic reticulum kinase( PERK)... [Objectives] To study the therapeutic effect and mechanism of New Maixian Powder on ulcerative colitis( UC) rats through observing its regulatory effect on the protein kinase R-like endoplasmic reticulum kinase( PERK)/eukaryotic translation initiation factor-2α( e IF-2α)/nuclear transcription factor-kappa B( NF-κB) signaling pathway. [Methods]First,60 SD rats were randomly divided into normal group,model group,mesalazine group,and New Maixian Powder low,medium and high dose groups,10 rats each group. Then,dextran sulfate sodium( DSS) was used to induce UC rats. The mesalazine group was given 0. 42 g/( kg·d) of mesalazine sustained-release granule suspension,New Maixian Powder low,medium and high dose groups were given 1. 5,3,and 6 g/( kg·d) of New Maixian Powder suspension,respectively,and other groups were given an equal volume of physiological saline,continuous intragastric administration for 14 d. Next,the disease activity index( DAI) of UC rats was evaluated; the expression of NF-κB in serum was measured by enzyme-linked immunosorbent assay( ELISA); the expression of PERK and e IF-2α protein and m RNA in colon tissue was detected by Western blot and real-time quantitative polymerase chain reaction( RT q-PCR). [Results] Compared with the normal group,the DAI score and serum NF-κB level in the model group were significantly higher( P < 0. 05),and PERK and e IF-2α protein and m RNA levels in the colon tissue were increased( P < 0. 05); compared with the model group,the DAI score decreased and serum NF-κB level declined in the New Maixian Powder group,and the expression of PERK and e IF-2α protein and m RNA in New Maixian Powder medium dose and high dose groups declined( P < 0. 05). [Conclusions]New Maixian Powder has good therapeutic effect on UC rats,and its mechanism may be connected with the inhibition of the activation of PERK/e IF-2α/NF-κB signaling pathway. 展开更多
关键词 New Maixian Powder Ulcerative colitis(UC) Protein kinase R-like endoplasmic reticulum kinase(PERK) Eukaryotic translation initiation factor-2α(eIF-2α) Nuclear transcription factor-kappa B(NF-κB)
下载PDF
Author Correction:Enhanced CD19 activity in B cells contributes to immunodeficiency in mice deficient in the ICF syndrome gene Zbtb24
2
作者 Zhengzhou Ying Swanand Hardikar +7 位作者 Joshua B.Plummer Tewfik Hamidi Bin Liu Yueping Chen jianjun shen Yunxiang Mu Kevin M.McBride Taiping Chen 《Cellular & Molecular Immunology》 SCIE CAS CSCD 2024年第1期100-100,共1页
In the sentence beginning‘To trace cell proliferation,FO and MZ B cells’and the sentence beginning‘For cell activation,naïve B cells or CH12F3 cells’in this article,the[10 ng/ml]‘F(ab’)_(2)fragment goat ant... In the sentence beginning‘To trace cell proliferation,FO and MZ B cells’and the sentence beginning‘For cell activation,naïve B cells or CH12F3 cells’in this article,the[10 ng/ml]‘F(ab’)_(2)fragment goat anti-mouse IgM’should have read‘10μg/ml F(ab’)_(2)fragment goat anti-mouse IgM’.The original article has been corrected. 展开更多
关键词 IMMUNODEFICIENCY CD19 DEFICIENT
原文传递
Enhanced CD19 activity in B cells contributes to immunodeficiency in mice deficient in the ICF syndrome gene Zbtb24
3
作者 Zhengzhou Ying Swanand Hardikar +7 位作者 Joshua B.Plummer Tewfik Hamidi Bin Liu Yueping Chen jianjun shen Yunxiang Mu Kevin M.McBride Taiping Chen 《Cellular & Molecular Immunology》 SCIE CAS CSCD 2023年第12期1487-1498,共12页
Immunodeficiency,centromeric instability,and facial anomalies(ICF)syndrome is a rare autosomal recessive disorder characterized by DNA hypomethylation and antibody deficiency.It is caused by mutations in DNMT3B,ZBTB24... Immunodeficiency,centromeric instability,and facial anomalies(ICF)syndrome is a rare autosomal recessive disorder characterized by DNA hypomethylation and antibody deficiency.It is caused by mutations in DNMT3B,ZBTB24,CDCA7,or HELLS.While progress has been made in elucidating the roles of these genes in regulating DNA methylation,little is known about the pathogenesis of the life-threatening hypogammaglobulinemia phenotype.Here,we show that mice deficient in Zbtb24 in the hematopoietic lineage recapitulate the major clinical features of patients with ICF syndrome.Specifically,Vav-Cre-mediated ablation of Zbtb24 does not affect lymphocyte development but results in reduced plasma cells and low levels of IgM,IgG1,and IgA.Zbtb24-deficient mice are hyper and hypo-responsive to T-dependent and T-independent type 2 antigens,respectively,and marginal zone B-cell activation is impaired.Mechanistically,Zbtb24-deficient B cells show severe loss of DNA methylation in the promoter region of Il5ra(interleukin-5 receptor subunit alpha),and Il5ra derepression leads to elevated CD19 phosphorylation.Heterozygous disruption of Cd19 can revert the hypogammaglobulinemia phenotype of Zbtb24-deficient mice.Our results suggest the potential role of enhanced CD19 activity in immunodeficiency in ICF syndrome. 展开更多
关键词 ICF syndrome ZBTB24 CD19 IL-5Ra HYPOGAMMAGLOBULINEMIA
原文传递
上一页 1 下一页 到第
使用帮助 返回顶部