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作 者:钱莉莉[1] 刘啸[2] QIAN Li- li;LI Xiao(Department of Stomatology, Second Affiliated Hospital of Xinfiang Medical University, Urumqi 830018, China)
机构地区:[1]安徽省滁州市第一人民医院北区口腔科,安徽滁州239000 [2]新疆医科大学二附院口腔科,新疆乌鲁木齐830018
出 处:《解剖学研究》2018年第2期104-107,共4页Anatomy Research
基 金:新疆维吾尔自治区自然科学基金(2017D01C253)
摘 要:目的探讨白念珠菌感染口腔上皮细胞诱导炎症细胞因子的产生机制。方法采用随机数字法将70只小鼠平均分为两组,每组包含35只受试小鼠,模型组建立小鼠口腔白念珠菌感染的体内模型,对照组不进行任何处理;感染5 d后比较两组受试小鼠菌落计数、炎症细胞因子表达水平以及TLR2、TLR4表达量。结果感染5 d后,模型组受试小鼠的菌落数以及白斑面积评分均明显高于对照组,两组间差异具有统计学意义(P<0.05);模型组受试小鼠血清TNF-α、IL-6水平明显高于对照组,TGF-β水平明显低于对照组,且差异具有统计学意义(P<0.05);模型组受试小鼠TLR2、TLR4 m RNA扩增带相对吸光度值明显高于对照组,且差异具有统计学意义(P<0.05)。结论白念珠菌感染口腔上皮细胞后炎症细胞因子表达水平增加,其机制可能与感染白念珠菌后,其菌体作用于TLRs进而引起细胞内信号转导相关。Objective To assess the mechanism of indticed inflammatory cytokines induced by candida albicans infection in oral epithelial ceils. Methods The 70 mice were divided into two groups on average, with 35 mice in each group, and the model group mice developed the body model of oral candida albicans infection, and the control group did not carry out any treatment. After infection with 5 d, the colony counting, the expression levels of inflammatory cytokines, and the TLR2, TLR4 expression levels in the two groups were compared. Results After infection with 5 d, the number of bacterial colony and white spot area in the model group were significantly higher than that in the control group, and the difference between the two groups was statistically significant (P〈0.05). The serum TNF-alpha and IL-6 in the model group were significantly higher than those in the control group, and the TGF - beta level was significantly lower than the control group, and the difference was statistically significant (P〈0.05). The relative expression of TLR2 and TLR4 mRNA in the model group was significantly higher than that in the control group, and the difference was statistically significant (P〈0.05). Conclusion Candida albicans infection of oral epithelial cells and inflammatory cytokine expression level increased, its mechanism may be related to c. albicans infection, the bacteria on the TLRs resulting in intracelluiar signal transduction.
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