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| 1 | Parthenolide inhibits LPS-induced inflammatory cytokines through the toll-like receptor 4 signal pathway in THP-1 cells显示文摘Parthenolide (PTL ) 显示出反煽动性的有势力和反癌症活动。在现在的学习, PTL 的活动的分子的机制在导致的 lipopolysaccharide (LPS ) 被探索人的白血病 monocytic THP-1 房间和人的主要单核白血球。3-(4,5-dimethylthiazol-2-yl )-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium 盐(山) 试金被用来在 THP-1 房间生存能力上分析 PTL 的效果。连接酶的 immunosorbent 试金被用来在导致 LPS 的煽动性的 cytokine 分泌物上决定 PTL 的效果。流动 cytometry 和量的即时聚合酶链反应被用来在导致 LPS 的像使用费的受体上估计 PTL 的效果 4 (TLR4 ) 表示。表明分子的 Phosphorylation 层次被西方的污点分析决定。结果显示出那 PTL < 12.5 M 显著地没影响 THP-1 房间生存能力。LPS 治疗导致了 interleukin (IL ) 的一条显著起来规定 -6, IL-1, IL-8, IL-12p40,肿瘤坏死因素 -- , IL-18,并且没有在里面 THP-1 房间。然而, PTL 以一种剂量依赖者方式禁止了这些 cytokines 的表示,与 1.0912.620 M 的 IC 50 价值。PTL 与由流动 cytometry 分析决定了的 1.373 M 的 IC 50 值堵住了 TLR4 表示,并且这堵住的效果在蛋白质和 mRNA 层次被验证。另外的分子的表情的细胞外的调整信号的 kinase 1/2 ,6月N终端 kinase , p38 ,原子因素 B ( NF-B ) p65 ,和 IB 和起来规定的 phosphorylation 层次的起来规定(可诱导的氮的氧化物 synthase , TLR4 ,并且 TNF 联系受体的因素 6 )由 LPS 导致了被 PTL 以一种剂量依赖者方式废除。PTL 的反煽动性的机制通过表明小径的调停 TLR4 的激活 mitogen 的蛋白质 kinase 和 NF-B 部分操作。因此, TLR4 可以是为反发炎治疗的一个新目标。 | Shuangshuang Li Xiangli Gao Xiaoxin Wu Zhigang Wu Linfang Cheng Lifen Zhu Dan Shen Xiangmin Tong | 2015 | Acta Biochimica et Biophysica Sinica2015，47，5： | 5 |
| 2 | Effects of volatile anesthetic preconditioning on expression of NFkB-regulated genes in aged rat myocardium显示文摘Volatile anesthetic preconditioning has been shown to be a potent way to provide myocardium protection against ischemia/reperfusion(I/R)injury;however,this cardioprotection is lost in senescent animal models and elderly patients.NFκB-regulated genes have been linked to myocardial I/R injury and anesthetic preconditioning.Here,we investigated NFκB activation related to anesthetic preconditioning in aging rat myocardium.Isolated,Langendorff perfused rat hearts from Fischer 344 male rats,24 months old,were randomly assigned to one of the three groups.The hearts of the control group were perfused with physiologic solution without any intervention.The hearts in the I/R group were subjected to 25 minutes ischemia and followed by 60 minutes reperfusion.The hearts in the treatment group were subjected to 10 minutes 2.5% sevoflurane,followed by 20 minutes washout and by 25 minutes ischemia and 60 minutes of reperfusion,respectively.Left ventricular developed pressure(LVDP)and left ventricular enddiastolic pressure(LVEDP)were measured.Western blot analysis was used to measure inhibitor of κB(IκB)and antiapoptotic genes:A1,ILP,c-IAP-2,Bcl-2,caspase 8 and caspase 9.Ischemia and reperfusion significantly decreased LVDP and increased LVEDP in aged rat hearts.Anesthetic preconditioning with sevoflurane did not change the effects I/R on LVDP and LVEDP,despite the fact that after treatment with anesthetic preconditioning,the levels of IκB,A1,ILP,caspase 8 and caspase 9 were significantly different compared to those of the control hearts.In conclusion,anesthetic preconditioning with sevoflurane does not improve myocardial systolic and diastolic functions.Our results suggest that the activation of NFκB regulated genes is different in the senescent myocardium and could account for loss of cardioprotection with aging. | Caiyun Zhong Hong Qiu Jun Chen Hong Liu | 2019 | The Journal of Biomedical Research2019，33，4： | 1 |
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