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Noriko Inagaki‐Katashiba Tomoki Ito Muneo Inaba Yoshiko Azuma Akihiro Tanaka Vien Phan Kayoko Kibata Atsushi Satake Shosaku Nomura 《European journal of immunology》2019,49(11):2051-2062
DCs and epithelial cell‐derived thymic stromal lymphopoietin (TSLP) have pivotal roles in allergic inflammation. TSLP stimulates myeloid DCs to express OX40‐ligand (OX40L) and CCL17, which trigger and maintain Th2 cell responses. We have previously shown that statins, which are HMG‐CoA reductase inhibitors, have the ability to suppress type I IFN production by plasmacytoid DCs. Here, we extended our previous work to examine the immunomodulatory effect of statins on allergic responses, particularly the TSLP‐dependent Th2 pathway induced by myeloid DCs. We found that treatment of TSLP‐stimulated DCs with either pitavastatin or simvastatin suppressed both the DC‐mediated inflammatory Th2 cell differentiation and CRTH2+CD4+ memory Th2 cell expansion and also repressed the expressions of OX40L and CCL17 by DCs. These inhibitory effects of statins were mimicked by treatment with either a geranylgeranyl‐transferase inhibitor or Rho‐kinase inhibitor and were counteracted by the addition of mevalonate, suggesting that statins induce geranylgeranylated Rho inactivation through a mevalonate‐dependent pathway. We also found that statins inhibited the expressions of phosphorylated STA6 and NF‐κB‐p50 in TSLP‐stimulated DCs. This study identified a specific ability of statins to control DC‐mediated Th2 responses, suggesting their therapeutic potential for treating allergic diseases. 相似文献
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Xuemei Huang MD PhD Alvaro Alonso MD PhD Xuguang Guo PhD David M. Umbach PhD Maya L. Lichtenstein MD Christie M. Ballantyne MD Richard B. Mailman PhD Thomas H. Mosley PhD Honglei Chen MD PhD 《Movement disorders》2015,30(4):552-559
Previous findings on the association of statins, plasma lipids, and Parkinson's disease (PD) are confounded by the fact that statins also affect lipid profiles. We prospectively examined plasma lipids and statin use in relation to PD in the Atherosclerosis Risk in Communities (ARIC) Study. Statin use and plasma lipids were assessed at baseline (visit 1, 1987‐89) and at three triennial visits thereafter (visits 2‐4) until 1998. Potential PD cases were identified from multiple sources and validated where possible. The primary analysis was limited to incident PD cases diagnosed between 1998 and 2008. Odds ratios and 95% confidence intervals were derived from multivariate logistic regression models. Statin use was rare at baseline (0.57%) but increased to 11.2% at visit 4. During this time frame, total‐cholesterol levels decreased, particularly among statin users. Fifty‐six PD cases were identified after 1998. Statin use before 1998 was associated with significantly higher PD risk after 1998 (odds ratio = 2.39, 95% confidence interval 1.11‐5.13) after adjusting for total cholesterol and other confounders. Conversely, higher total cholesterol was associated with lower risk for PD after adjustment for statin usage and confounders. Compared with the lowest tertile of average total cholesterol, the odds ratios for PD were 0.56 (0.30‐1.04) for the second and 0.43 (0.22‐0.87) for the third tertile (Ptrend = 0.02). Statin use may be associated with a higher PD risk, whereas higher total cholesterol may be associated with lower risk. These data are inconsistent with the hypothesis that statins are protective against PD. © 2015 International Parkinson and Movement Disorder Society 相似文献
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他汀类药物对癌症患者预后的 Meta 分析(英文) 总被引:1,自引:0,他引:1
目的:系统评价癌症患者服用他汀类药物后对疾病预后的作用。方法:利用计算机检索Cochrane Library,
PubMed和EMbase数据库,收集这些数据库中从建库至2015年3月公开发表的有关他汀类药物和癌症预后的文章,采
用Stata 12.0软件进行Meta分析。结果:共纳入25篇文献,523 193例患者。Meta分析结果显示:与未服用他汀类药物的
癌症患者相比,服用他汀类药物的癌症患者的总体死亡危险比(hazard ratio,HR)为0.82(95% CI:0.76~0.89)。亚组分析
结果显示前列腺癌症患者死亡的HR为0.66(95% CI:0.52~0.83)。敏感性分析显示在排除随访时间<5年的文献后,服用
他汀类药物的癌症患者的死亡HR为0.91(95% CI:0.75~1.10)。结论:他汀类药物能在一定程度上降低癌症患者的病死
率,但其远期作用还需要进一步研究确认。 相似文献
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《The Journal for Nurse Practitioners》2021,17(8):910-915
The purpose of this report is to inform nurse practitioners and other health care providers about how to treat dyslipidemia in the statin-intolerant patient while simultaneously achieving optimal cardiovascular outcomes for this patient population. This report will briefly explain how to rechallenge the statin-intolerant patient and the secondary therapies that are available to decrease cardiovascular morbidity and mortality. Algorithms for rechallenging the statin-intolerant patient and secondary therapies are also provided. 相似文献
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