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机构地区:[1]河南中医学院老年医学研究所,河南郑州450008
出 处:《时珍国医国药》2012年第7期1693-1694,共2页Lishizhen Medicine and Materia Medica Research
基 金:国家"973"重点基础研究发展计划(No.2006CB504605);河南省高校新世纪优秀人才支持计划(No.2006HANCET-05)
摘 要:目的探讨毒素清对肺炎痰热证大鼠肺组织TLR4、NF-κB的影响,以揭示毒素清治疗肺炎痰热证的作用机制。方法制备细菌性肺炎痰热证模型,将Wistar大鼠随机分为正常组、肺炎组、肺炎痰热证组、阳性对照组、毒素清组。采用免疫组化法测定各组肺组织TLR4、NF-κB的表达。结果与正常组比较,肺炎组、肺炎痰热证组肺组织TLR4、NF-κB表达水平显著升高(P<0.01),其中,肺炎痰热证组较肺炎组升高明显(P<0.01);与肺炎痰热证组相比,毒素清组、阳性对照组肺组织TLR4、NF-κB表达明显减弱(P<0.01),其中,毒素清组肺组织NF-κB表达与阳性对照组相比减弱尤为明显(P<0.05),TLR4表达与阳性对照组相比有降低的趋势,但无统计学意义。结论 TLR4、NF-κB通路参与了肺炎痰热证肺组织的病理损伤过程;毒素清治疗肺炎痰热证的作用机制可能是通过抑制TLR4、NF-κB的表达,从而起到减轻肺损伤的作用。Objective To investigate influence of Dusuqing(DSQ),a traditional Chinese medicine prescription on expression of toll-like receptor 4(TLR4)and nuclear factor κB(NF-κB) in lung tissue of rat models with bacterial pneumonia and phlegm-heat syndrome and to reveal the mechanism of DSQ in treatment of the disease. Methods Wistar rats were randomized into five groups:normal,pneumonia,pneumonia with phlegm-heat syndrome,positive control and DSQ treated groups.Rat models with bacterial pneumonia accompanied with Phlegm-heat syndrome were made.The expressions of TLR4 and NF-κB proteins in lung tissue were analyzed by immunohistochemistry staining. Results The expressions of TLR4 and NF-κB in pneumonia group and pneumonia with phlegm-heat syndrome group were markedly higher than those in normal control group(P〈0.01).And in pneumonia with phlegm-heat syndrome group the expressions of TLR4 and NF-κB were significantly higher than those in the pneumonia group(P〈0.01).Compared with pneumonia with phlegm-heat syndrome group,the expressions of TLR4 and NF-κB were markedly weakened in positive control group and DSQ treated group(P〈0.01)and the expressions of NF-κB in DSQ treated group were weakened significantly than those in positive control group(P〈0.05). Conclusion TLR4,NF-κB signal transduction pathway was involved in the pathological changes of lung tissues in pneumonia with phlegm-heat syndrome.The mechanism of DSQ in treating bacterial pneumonia with phlegm-heat syndrome may be related to its ability of suppressing of TLR4 and NF-κB expression.
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