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作 者:于振香[1] 彭丽萍[1] 左梦华[1] 赵雪俭[2]
机构地区:[1]吉林大学第一医院呼吸内科,吉林长春130021 [2]吉林大学基础医学院病理生理学研究室
出 处:《中国老年学杂志》2007年第3期208-210,共3页Chinese Journal of Gerontology
基 金:吉林省自然科学基金资助课题(20030551-3)
摘 要:目的探讨人参二醇皂苷(PDS)对“二次打击”全身炎症反应综合征(SIRS)肺损伤保护作用的分子机制。方法Wistar大鼠随机分为假手术对照组(S组)、失血-内毒素二次打击组(HL组)、地塞米松预治疗组(HLD)及PDS预治疗组(HLP组)。大鼠经失血性休克引起的“一次打击”和内毒素引起的“二次打击”后,导致SIRS模型。提取肺总RNA和蛋白,分别以RT-PCR检测CD14和IκBa mRNA表达,应用Western blot检测CD14和NF-κB的蛋白表达。结果肺组织CD14 mRNA和蛋白质表达丰度以HL组最高,HLP组、HLD组均明显低于HL组(P<0.05)。而IκBamRNA表达水平,HL组明显低于S组(P<0.01),HLP组和HLD组明显高于HL组(P<0.05和P<0.01),而与S组相近(P>0.05)。HL组的NF-κBP65蛋白质表达水平明显高于S组,HLD和HLP组的NF-κBP65蛋白质表达水平也低于HL组(P<0.05),接近S组(P>0.05)。结论PDS与DEX对“两次打击”SIRS肺损伤有类似的保护作用,抑制LPS介导的CD14和NF-κB信号转导通路的过度激活是实现对肺保护作用的重要机制。Objective To explore the molecular mechanism of protective effects of panaxadiol saponins (PDS) on lung tissues of the two-hit rat models with systemic inflammatory reaction syndrome (SIRS). Methods Wistar rats were randomly divided into sham operational (S) group; two-hit with hemorrage and lipopolysaccharide (LPS) (HL) group; dexamethasone (DEX) pretreatment (HLD) group; PDS pretreatment (HLP) group. The rat models with SIRS were made by hemorrage shock as the first hit and with endotoxin as the second hit, then the expressions of CD14 and IκBa mRNA were measured by semi-quantitative reverse transcriptase polymerase chain reaction ( RT- PCR) and the expressions of CD14 and NF-κB proteins were determined by Western blotting assay. Results The expressions of CD14 mRNA and protein in HL group were significantly highest, that in HLP, HLD group was lower than that in HL group ( P 〈 0.05 ). The expression of lung IκBa mRNA in HL group was significantly lower than that in S group ( P 〈0. 01 ) , while that in HLD and HLP group were higher than that in HL group( P 〈0.05 and P 〈0.01 ), but similar to that in S group ( P 〉 0. 05 ). The expression of NF-κB P65 protein in HL group was significantly higher than that in S group ( P 〈 0. 05 ) , while that in HLP and HLD group were lower than that in HL group ( P 〈 0. 05 ) , close to that in S group ( P 〉 0. 05 ). Conclusions PDS and DEX have similar protective effect on SIRS lung damage by two-hit. To inhibit the over activation of NF-κB signal transduction way induced by LPS is the important mechanism of lung protection.
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