机构地区:[1]吉林大学基础医学院病理生理学研究室
出 处:《吉林大学学报(医学版)》2005年第2期231-235,共5页Journal of Jilin University:Medicine Edition
基 金:吉林省科技厅自然科学基金资助课题 (2 0 0 30 5 5 1- 3) ;吉林省科技厅自然科学基金攻关课题 (2 0 0 30 5 0 1)
摘 要:目的 :探讨人参二醇皂苷 (PDS)对内毒素休克肺损伤保护作用的分子机制。方法 :Wistar大鼠随机分为实验对照组 (CTRG)、内毒素 (L PS)休克组 (L PSG)、人参二醇皂苷组 (PDSG)和地塞米松组 (DEXG)。以内毒素 (4mg· kg- 1 )复制内毒素休克模型 ,平均动脉压降至基础血压的 2 / 3为休克状态。取肺组织光镜下进行形态学观察 ,提取肺总 RNA和蛋白 ,分别以 RT- PCR检测 CD14和 IκBα m RNA表达 ,应用 Western blotting检测 CD14和 NF- κB的蛋白表达。结果 :1肺组织的病理学变化 ,L PSG可见弥漫性间质炎性改变 ,肺泡壁明显增宽 ,肺泡腔含气量明显减少 ,很多肺泡腔内有渗出液。 PDSG和 DEXG的病变显著轻于 L PSG;2肺组织CD14 m RNA和蛋白质表达丰度以 L PSG最高 ,PDSG与 DEXG均明显低于 L PSG (P<0 .0 5 ) ,而与 CTRG相近(P>0 .0 5 )。 IκBα m RNA表达水平 ,L PSG明显低于 CTRG (P<0 .0 1) ,PDSG与 DEXG明显高于 L PSG(P<0 .0 5和 P<0 .0 1) ,而与 CTRG相近 (P>0 .0 5 )。 L PSG的 NF- κB P6 5蛋白质表达水平明显高于 CTRG,PDSG与 DEXG的 NF- κB P6 5蛋白质表达水平也低于 L PSG(P<0 .0 5 ) ,接近 CTRG(P>0 .0 5 )。结论 :PDS与DEX对内毒素休克肺损伤有类似的保护作用 ,抑制 L PS介导的 CD14 - NF-Objective To explore the molecular mechanism of protective effects of Panaxadiol Saponins (PDS) on lung tissues of endotoxic shock rats. Methods Wistar rats were randomly divided into control group (CTRG), lipopolysaccharide (LPS) shock group (LPSG), LPS shock+dexamethasone group (DEXG) and LPS shock+PDS group (PDSG), respectively. Endotoxin shock models were duplicated by injection of LPS (4 mg·kg~ -1). The histological changes of the lung tissues stained with hematoxylin and eosin (HE) among four groups were compared through microscopic examination. Meanwhile, the expressions of CD14 and IκBα 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 ①The histological and pathological changes: in LPSG, there was the effusion of a large amount of lymphocytes, mono-macrophages and neutrophils around the alveolar and vascular walls; incrassated alveolar septums and bronchiole walls were caused by hyperemia ,edema and infiltration of pulmonary interstitial;focal atrophia and formation of pneumatocele could be observed; only small amount of alveolus containing air could be found; however, the lung pathologic changes in DEXG and PDSG were significantly slighter than those in LPSG, and they merely showed slight effusion of inflammatory cells, and the content of air in alveolus was near to that in CTRG. ②The expressions of CD14 mRNA and protein in LPSG were significantly higher than those in CTRG(P<0.05), while those in DEXG and PDSG were close to those in CTRG(P>0.05), significantly lower than those in LPSG(P<0.05). The expression of lung IκBα mRNA in LPSG was significantly lower than those in CTRG(P<0.01), while those in DEXG and PDSG were close to that in CTRG(P>0.05) and higher than that in LPSG(P<0.05 and P<0.01). The expression of NF-κB P65 protein in LPSG was significantly strengthened than that in CTRG(P<0.05), while those in PDSG and DEXG were lower than tha
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