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作 者:金晓凤[1] 徐正衸[1] 王万铁[1] 许益笑[1] 张晓隆[1]
机构地区:[1]温州医学院病理生理学教研室,浙江温州325035
出 处:《中国应用生理学杂志》2009年第1期41-44,共4页Chinese Journal of Applied Physiology
基 金:浙江省卫生厅科研基金资助项目(SWS00021)
摘 要:目的:研究家兔肺缺血/再灌注损伤时Toll样受体4(TLR4)信号转导通路变化及虎杖甙(PD)对其影响。方法:复制在体肺缺血/再灌注损伤模型。健康日本大耳白免30只,随机分为对照(C)组、缺血/再灌注(I/R)组、PD组。鲎试剂试管法检测血浆内毒素(ET);RT-PCR法检测肺组织TLR4、核因子-κBp65(NF-κBp65)和细胞间粘附分子-1(ICAM-1)mRNA表达;苏木素-伊红(HE)染色,光镜观察肺组织形态学变化。结果:I/R组、PD组与C组相比血浆ET无显著差异(均P>0.05)。L/R组肺组织TLR4、NF-κBp65及ICAM-1mRNA表达较C组显著升高(均P<0.01); PD组上述改变较L/R组明显下降,但仍高于C组(均P<0.01);光镜见PD组肺组织结构损伤明显轻于I/R组。结论:PD治疗可以下调肺组织TLR4、NF-κBp65表达,进而抑制ICAM-1等炎症介质的转录和分泌,减轻肺缺血/再灌注损伤。Aim: To investigate protective effects of polydatin(PD) during lung ischemia/reperfusion in rabbits and its potential inechanisms. Me thods: Rabbit lung modal of ischemia/reperfusion(I/R) injury was constituted in vivo. Thirty rabbits were divided into groups randomly: Control( C), I/R, PD group, respectively. Endotoxin(ET) in plasma was analyzed by End-point Chromogenic Assay, the expression of Toll-like receptor 4(TLR4) mRNA, nuclear factor(NF)-KBp65 mRNA, intracellular adhesion molecule-1 (ICAM-1) mRNA were measured by RT-PCR, the morphological changes of lung tissue were observed with hematoxylin-eosin (HE) staining. Results: There was no significant difference in ET concentration of plasma between groups (all of P 〉 0.05). The expression of TLR-4 mRNA, NF-KBp65 mRNA and ICAM-1mRNA in I/ R group were significantly increased as compared to C group and PD group, while those expressions in PD group were evidently higher than those in C group(all of P 〈 0.01). Light microscope sbow'ed that the lung pathological injuries in PD group were obviously alleviated as compared to I/R group. Conclusion: PD might have a protective effect on lung ischemia/reperfusion injury by down-regulating TLR4 and NF-KB expression, then inhibiting the release of mediators of inflan,nation as ICAM- 1.
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