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The Mechanism Of Portulaca Attenuates Development Of Dextran Sulfate Sodium Induced Colitis In Mice

Posted on:2019-08-05Degree:MasterType:Thesis
Country:ChinaCandidate:R KongFull Text:PDF
GTID:2394330545973419Subject:Clinical medicine
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Objective To investigate the protective effect of portulaca extract on ulcerative colitis in mice induced by dextran sulfate sodium(DSS)and its mechanism.Methods Mice were divided into 4 groups using a random number table:(1)Normal control: given normal food and water for 7 days,(2)DSS group: 3% DSS + saline by gavage for 7 days,(3)Mesalamine positive control group: 3% DSS + 7.4mg/kg mesalamine daily by gavage for 7 days,(4)Portulaca group:3% DSS+ 100mg/kg daily by gavage for 7 days.During the period of modeling,mice weight,stool form,and stool occult blood were recorded every day to assess the disease activity index(DAI)of ulcerative colitis.After 7 days,the mice were killed by anesthesia and intestinal segment was collected from the cecum to the anal.The colorectal length was measured and several indexes of different groups of mice were evaluated through disease activity index(DAI),histological scores,serum inflammatory cytokines(TNF-?,IL-6,IL-1?)and myeloperoxidase(myeloperoxidase,MPO).Furthermore,to explore the protective mechanism of purslane extract on DSS-induced murine ulcerative colitis,we detected the expression level of intercellular PPAR-? and NF-?B pathway using western blot(WB),real-time reverse transcriptase polymerase chain reaction(qRT-PCR)and immunohistochemical staining(IHC).Results The determination results of the pro-inflammatory cytokines,DAI and MPO levels,NF-?B and PPAR-? activity,the expression of Bcl-2/Bax activity between the 4 groups had statistical significance in varying degrees.Conclusion The portulaca extract has protective effect on ulcerative colitis in mice induced by DSS,and it can significantly oppresse the apoptosis and activation of NF-?B induced by DSS via activating PPAR-?.
Keywords/Search Tags:Portulacase, dextran sulfate sodium, inflammatory bowel disease, PPAR?, apoptosis
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