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1.
Eur Rev Med Pharmacol Sci ; 23(14): 6371-6378, 2019 Jul.
Article in English | MEDLINE | ID: mdl-31364145

ABSTRACT

OBJECTIVE: To investigate the influences of probiotics combined with sulfasalazine (SASP) on the expression of the Wnt/ß-catenin signaling pathway in rats with ulcerative colitis (UC). MATERIALS AND METHODS: A total of 60 clean level and healthy Sprague-Dawley (SD) rats were randomly divided into the normal group, model group, SASP group and combination therapy group, with 15 rats in each group. The rats in the normal group were given normal feeding, and those in the remaining three groups were subjected to the establishment of the UC model. During the modeling, the rats underwent daily gavage and were sacrificed after 4 weeks. Clinical symptoms and pathological changes in ulcer indexes and colon tissues were observed in each group. The expression levels of relative genes in the Wnt/ß-catenin signaling pathway were detected by Polymerase Chain Reaction (PCR). RESULTS: Compared with those in the model group, the pathological sections of rats in the SASP group and combination therapy group showed significant improvement in the inflammatory response. The expression levels of relative genes in the Wnt/ß-catenin signaling pathway were downregulated in rats of the SASP group and combination therapy group relative to those in the model group. CONCLUSIONS: SASP and probiotics alleviate UC by reducing inflammation by inhibiting the activation of the Wnt/ß-catenin signaling pathway, thereby improving intestinal function and restoring the intestinal structure.


Subject(s)
Colitis, Ulcerative/drug therapy , Probiotics/administration & dosage , Sulfasalazine/administration & dosage , Wnt Signaling Pathway/drug effects , Animals , Colitis, Ulcerative/metabolism , Disease Models, Animal , Drug Therapy, Combination , Gene Expression Regulation/drug effects , Male , Probiotics/pharmacology , Rats , Rats, Sprague-Dawley , Sulfasalazine/pharmacology , Treatment Outcome
2.
Eur Rev Med Pharmacol Sci ; 23(5): 2151-2157, 2019 Mar.
Article in English | MEDLINE | ID: mdl-30915760

ABSTRACT

OBJECTIVE: To study the effect of micro ribonucleic acid (miR)-146a on the development of ulcerative colitis (UC) and to explore its regulatory effect on the Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88) and nuclear factor-kappa B (NF-κB) signaling pathways. MATERIALS AND METHODS: The UC model in rats was established using 2,4,6-trinitrobenzenesulfonic acid (TNBS)/ethanol. A total of 30 male rats were randomly divided into control group, model group and miR-146a inhibitor group, with 10 rats in each group. The disease activity index (DAI) and the macroscopic score of colonic mucosa were measured in each rat. MiR-146a expression in rat intestinal tissues was detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). Serum levels of interleukin-1ß (IL-1ß) and tumor necrosis factor-α (TNF-α) in rats were detected via enzyme-linked immunosorbent assay (ELISA). Additionally, Western blotting assay was performed to detect protein levels of TLR4, MyD88, and NF-κB in rat intestinal tissues. RESULTS: Compared with those in control group, rats in model group had notably increased DAI, inflammation score, upregulated expression levels of TLR4, MyD88, NF-κB, and miR-146a, as well as increased serum levels of IL-1ß and TNF-α. However, rats in miR-146a inhibitor group exhibited substantially decreased DAI, inflammation score, lowered content of IL-1ß and TNF-α and levels of TLR4, MyD88, and NF-κB compared with those in model group. CONCLUSIONS: We found that miR-146a inhibitor alleviates UC by reducing the release of inflammatory factors through suppressing the TLR4/MyD88/NF-κB signaling pathway.


Subject(s)
Colitis, Ulcerative/genetics , MicroRNAs/genetics , Signal Transduction , Trinitrobenzenesulfonic Acid/adverse effects , Animals , Colitis, Ulcerative/chemically induced , Colitis, Ulcerative/metabolism , Disease Models, Animal , Gene Expression Regulation , Male , Myeloid Differentiation Factor 88/metabolism , NF-kappa B/metabolism , Random Allocation , Rats , Toll-Like Receptor 4/metabolism
3.
HLA ; 91(6): 543-544, 2018 06.
Article in English | MEDLINE | ID: mdl-29464869
4.
HLA ; 91(4): 303-305, 2018 04.
Article in English | MEDLINE | ID: mdl-29292580

ABSTRACT

HLA-B*40:338N differs from HLA-B*40:01:01 by a single nucleotide substitution at position 843C>A.


Subject(s)
Alleles , Asian People/genetics , HLA-B Antigens/genetics , Leukemia/genetics , Base Sequence , Exons/genetics , Humans , Sequence Alignment
5.
HLA ; 91(2): 136-137, 2018 02.
Article in English | MEDLINE | ID: mdl-29193787

ABSTRACT

HLA-B*27:04:06 differs from HLA-B*27:04:01 by a single-nucleotide substitution at position 396 C > A.


Subject(s)
Alleles , Asian People/genetics , Bone Marrow/metabolism , HLA-B Antigens/genetics , Tissue Donors , Base Sequence , Exons/genetics , Humans
6.
HLA ; 91(2): 133-134, 2018 02.
Article in English | MEDLINE | ID: mdl-29243881

ABSTRACT

HLA-B*13:98 differs from HLA-B*13:02:01 by a single nucleotide substitution at position 193 A>G.


Subject(s)
Alleles , Asian People/genetics , HLA-B Antigens/genetics , Base Sequence , Exons/genetics , Humans
7.
HLA ; 91(2): 142-143, 2018 02.
Article in English | MEDLINE | ID: mdl-29220119

ABSTRACT

HLA-DQB1*03:181 has one nucleotide change from HLA-DQB1*03:05:01 at position 470C>G.


Subject(s)
Alleles , Asian People/genetics , HLA-DQ beta-Chains/genetics , Leukemia/genetics , Base Sequence , Exons/genetics , Humans
8.
HLA ; 90(2): 118-120, 2017 08.
Article in English | MEDLINE | ID: mdl-28371366

ABSTRACT

HLA-B*40:01:41 differs from HLA-B*40:01:01 by a single nucleotide substitution at position 195 G>A.


Subject(s)
Alleles , Genotyping Techniques , HLA-B40 Antigen/genetics , Polymerase Chain Reaction , Asian People , Blood Donors , Fetal Blood , Humans
11.
HLA ; 89(1): 64-65, 2017 Jan.
Article in English | MEDLINE | ID: mdl-27885833

ABSTRACT

HLA-DRB1*08:69 has one nucleotide change from HLA-DRB1*08:03:02 at position 262 G>A.

15.
Zhonghua Nei Ke Za Zhi ; 55(7): 541-3, 2016 Jul 01.
Article in Chinese | MEDLINE | ID: mdl-27373290

ABSTRACT

Based on high throughput sequencing and PCR detection technology, this study has found out that intestinal microbial diversity was impaired and the quantities of two main bacteria flora (Bacteroidetes and Clostridium) were significantly reduced in patients with diarrhea-predominant irritable bowel syndrome (D-IBS). Meanwhile mucosal expression of toll-like receptor (TLR) 2 and TLR4 were significantly enhanced, which was inversely correlated with the reduction of Bacteroidetes and Clostridium. Thus, it suggests that D-IBS may be associated with TLR signal transduction triggered by the intestinal dysbacteriosis.


Subject(s)
Diarrhea/genetics , Intestinal Mucosa/metabolism , Irritable Bowel Syndrome/genetics , Toll-Like Receptor 2/genetics , Toll-Like Receptor 4/genetics , Adult , Base Sequence , Case-Control Studies , Diarrhea/metabolism , Female , Gene Expression/genetics , Humans , Male , Middle Aged , Polymerase Chain Reaction , Sequence Analysis, RNA/methods , Signal Transduction , Toll-Like Receptor 2/metabolism , Toll-Like Receptor 4/metabolism
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