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Effects Of Active Peptide From The Bombina Maxima On Cytokines?cytokine And Survival RAW264.7 In Mice

Posted on:2020-01-05Degree:MasterType:Thesis
Country:ChinaCandidate:T H LiFull Text:PDF
GTID:2404330602456343Subject:Surgery
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[Objective]To investigate the effects of Bombina maxima active peptide on RAW264.7 cytotoxicity,cytokine and survival rate of inflammatory response in mice.[Methods]RAW264.7 cells were treated with different concentrations of K-peptide and polymyxin B.The cell survival rate of RAW264.7 cells treated with different concentrations of drugs was measured by MTS after 2 hours.RAW264.7 cells were induced to produce different cytokines by LPS solution.The effects of different concentrations of K-peptide on IL-6 and TNF-alpha cytokines were detected by ELISA kit 24 hours later.The mice were randomly divided into blank group,control group and experimental group.The control group was injected with LPS solution,while the experimental group was injected with LPS solution containing K-peptide The survival rates of mice were counted within 24,48 and 72 hours respectively.[Results]Compared with polymyxin B group,the toxicity of K-peptide to RAW264.7 cells was significantly lower than that of polymyxin B group(P<0.01).Compared with LPS group,K-peptide could decrease the content of IL-6 in RAW264.7 cell supermatant(P<0.01)and the content of TNF-?(P<0.05).Compared with the control group,K-peptide decreased the nortality of mice and prolonged the survival time of mice with systemic inflammatory response(P<0.01).[Conclusion]The toxicity of K-peptide to RAW264.7 cells was significantly lower than that of polymyxin B at the same dose.K-peptide can decrease the content of IL-6?TNF-? in RAW264.7 cell supernatant.Increasing the survival rate of mice with LPS-induced inflammatory response may be related to reducing the content of IL-6?TNF-? in vivo and neutralizing LPS with K-peptide,thus alleviating systemic inflammatory response In mice.
Keywords/Search Tags:sepsis, active peptide, cytokines, inflammatory response
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