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首页> 外文期刊>VASA: Zeitschrift fuer Gefarsskrankheiten. Journal for vascular diseases >Tanshinone IIA attenuates elastase-induced AAA in rats via inhibition of myD88-dependent TLR-4 signaling [Tanshinone IIA schw?cht das elastase-induzierte bauch-aortenaneurysma in ratten über eine hemmung der myD88-abh?ngige TLR-4 signalsierung ab]
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Tanshinone IIA attenuates elastase-induced AAA in rats via inhibition of myD88-dependent TLR-4 signaling [Tanshinone IIA schw?cht das elastase-induzierte bauch-aortenaneurysma in ratten über eine hemmung der myD88-abh?ngige TLR-4 signalsierung ab]

机译:丹参酮IIA通过抑制myD88依赖性TLR-4信号传导减弱大鼠的弹性蛋白酶诱导的AAA [丹参酮IIA通过抑制myD88依赖性TLR-4信号传导减弱大鼠的弹性蛋白酶诱导的腹主动脉瘤。

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摘要

Background: The purpose of this study was to determine whether myeloid differentiation factor88-dependent Toll-Like Receptor-4 (TLR-4) signaling contributed to the inhibition of abdominal aortic aneurysm (AAA) by Tanshinone IIA (Tan IIA). Materials and methods: Male Sprague-Dawley rats (n = 12/group) were randomly distributed into three groups: Tan IIA, control, and sham. The rats from Tan IIA and control groups under-went intra-aortic elastase perfusion to induce AAAs, and those in the sham group were perfused with saline. Only the Tan IIA group received Tan IIA (2 mg/rat/d). Aortic tissue samples were harvested at 24 d after perfusion and evaluated using reverse transcriptase-polymerase chain reaction, Western blot, immunohistochemistry and immunofluorescence. Results: The over-expression of Toll-Like Receptor-4 (TLR-4), Myeloid Differentiation factor 88 (MyD88), Phosphory-lated Nuclear Factor κB (pNF-κB) and Phosphorylated IκBα (pIκBα) induced by elastase perfusion were significantly decreased by Tan IIA treatment. Conclusions: Tan IIA attenuates elastase-induced AAA in rats possibly via the inhibition of MyD88-dependent TLR-4 signaling, which may be one potential explanation of why Tan IIA inhibits AAA development through multiple effects.
机译:背景:这项研究的目的是确定是否依赖于髓样分化因子88的Toll样受体4(TLR-4)信号是否有助于丹参酮IIA(Tan IIA)抑制腹主动脉瘤(AAA)。材料和方法:将雄性Sprague-Dawley大鼠(每组12只)随机分为三组:Tan IIA,对照组和假组。 Tan IIA和对照组的大鼠进行主动脉内弹性蛋白酶灌注以诱导AAA,而假手术组的大鼠则灌注生理盐水。仅Tan IIA组接受Tan IIA(2 mg /大鼠/天)。灌注后第24天收集主动脉组织样品,并使用逆转录酶-聚合酶链反应,Western印迹,免疫组织化学和免疫荧光进行评估。结果:弹性蛋白酶灌注显着诱导了Toll样受体4(TLR-4),髓样分化因子88(MyD88),磷酸化核因子κB(pNF-κB)和磷酸化IκBα(pIκBα)的过表达。 Tan IIA治疗可降低。结论:Tan IIA可能通过抑制MyD88依赖的TLR-4信号传导来减弱大鼠的弹性蛋白酶诱导的AAA,这可能是为什么Tan IIA通过多种作用抑制AAA发育的一种可能的解释。

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