Low-dose NSAIDs reduce pain via macrophage targeted nanoemulsion delivery to neuroinflammation of the sciatic nerve in rat.

Low-dose NSAIDs reduce pain via macrophage targeted nanoemulsion delivery to neuroinflammation of the sciatic nerve in rat.
复制标题

DOI:
10.1016/j.jneuroim.2018.02.010
复制
发表时间:
2018-05-15
影响因子:
3.3
通讯作者:
Pollock JA
Pollock JA
中科院分区:
医学4区
文献类型:
--
作者:
Janjic JM;Vasudeva K;Saleem M;Stevens A;Liu L;Patel S;Pollock JA

文献摘要

参考文献

被引文献

相似文献

涉及巨噬细胞的神经炎症升高与神经性疼痛相关的前列腺素E2。用非甾体抗炎药(NSAID)治疗可抑制环氧合酶,减少PGE 2。然而,NSAID引起生理并发症。我们开发了包含塞来昔布和近红外染料的纳米乳剂。静脉注射的纳米乳剂被掺入在损伤处积聚的单核细胞中;在活体动物中通过荧光显示。单次给药(塞来昔布0.24 mg/kg)可在慢性压迫性损伤大鼠中提供靶向给药,导致可视化炎症、巨噬细胞浸润、考克斯-2和PGE 2显著减少。动物表现出持续至少4天的超敏反应缓解。与口服药物递送相比,药物的总身体负荷减少> 2000倍。
Neuroinflammation involving macrophages elevates Prostaglandin E2, associated with neuropathic pain. Treatment with non-steroidal anti-inflammatory drugs (NSAIDs) inhibits cyclooxygenase, reducing PGE2. However, NSAIDs cause physiological complications. We developed nanoemulsions incorporating celecoxib and near infrared dye. Intravenous injected nanoemulsion is incorporated into monocytes that accumulate at the injury; revealed in live animals by fluorescence. A single dose (celecoxib 0.24 mg/kg) provides targeted delivery in chronic constriction injury rats, resulting in significant reduction in the visualized inflammation, infiltration of macrophages, COX-2 and PGE2. Animals exhibit relief from hypersensitivity persisting at least four-days. The total body burden of drug is reduced by > 2000 fold over oral drug delivery.
DOI: 10.1038/nri2528
发表时间: 2009-04
期刊: Nature reviews. Immunology
影响因子: --
作者:
通讯作者: --
DOI: 10.2174/156720105774370267
发表时间: 2005-10-01
影响因子: 2.4
作者:
Sarker, Dipak K.
通讯作者: Sarker, Dipak K.
DOI: 10.1016/j.expneurol.2003.09.015
发表时间: 2004-01-01
影响因子: 5.3
作者:
Schäfers, M;Marziniak, M;Sommer, C
通讯作者: Sommer, C
DOI: 10.7150/thno.9476
发表时间: 2015
期刊: Theranostics
影响因子: 12.4
作者:
Patel SK;Janjic JM
通讯作者: Janjic JM
DOI: 10.1016/j.jneuroim.2015.04.012
发表时间: 2015-06-15
影响因子: 3.3
作者:
Vasudeva, Kiran;Vodovotz, Yoram;Azhar, Nabil;Barclay, Derek;Janjic, Jelena M.;Pollock, John A.
通讯作者: Pollock, John A.