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右酮洛芬在口腔面部疼痛中的药理特性

Pharmacological profile of dexketoprofen in orofacial pain.

作者信息

Miranda Hugo F, Sierralta Fernando, Aranda Nicolás, Noriega Viviana, Prieto Juan Carlos

机构信息

Faculty of Medicine, School of Pharmacy, Andrés Bello University, Santiago, Chile; Pharmacology Program, ICBM, Faculty Santiago, Chile of Medicine, University of Chile, Santiago, Chile.

Pharmacology Program, ICBM, Faculty Santiago, Chile of Medicine, University of Chile, Santiago, Chile; Faculty of Odontology, Finis Terrae University, Providencia, Chile.

出版信息

Pharmacol Rep. 2016 Dec;68(6):1111-1114. doi: 10.1016/j.pharep.2016.06.015. Epub 2016 Jun 25.

Abstract

BACKGROUND

Non-steroidal anti-inflammatory drugs (NSAIDs) may act through others mechanisms, in addition to inhibition of prostaglandin synthesis. These includes cholinergic, NO, serotonergic and opioids pathways.

METHODS

The aim of this work was to evaluate the effect of systemic action of (S)-+-ketoprofen (dexketoprofen, DEX) on pain behaviors using the orofacial formalin test in mice and the potential involvement of cholinergic, NO, serotonergic and opioids pathways.

RESULTS

The pretreatment of the mice with 1mg/kg ip of atropine or opoid antagonists: 1mg/kg, ip of NTX or 1mg/kg ip of NTI or 1mg/kg of NOR-BNI ip, did not produce significant change in the ED values of the antinociception to orofacial test induced by DEX. The pretreatment of the mice with 0.5mg/kg ip tropisetron, increased in a significant fashion the values of ED of DEX. When the mice were treated with 5mg/kg ip of L-NAME or 25mg/kg ip of aminoguanidine or 50mg/kg ip of 7-nitroindazole reversed the antinociception of DEX.

CONCLUSION

The findings of this study demonstrate activation of NO and 5-HTpathways play important roles in the systemic antinociceptive effect of DEX in a murine model of inflammatory pain.

摘要

背景

非甾体抗炎药(NSAIDs)除抑制前列腺素合成外,可能通过其他机制发挥作用。这些机制包括胆碱能、一氧化氮(NO)、5-羟色胺能和阿片类途径。

方法

本研究旨在通过小鼠口腔面部福尔马林试验评估(S)-(+)-酮洛芬(右酮洛芬,DEX)全身作用对疼痛行为的影响,以及胆碱能、NO、5-羟色胺能和阿片类途径的潜在参与情况。

结果

用1mg/kg腹腔注射阿托品或阿片拮抗剂对小鼠进行预处理:1mg/kg腹腔注射纳曲酮(NTX)或1mg/kg腹腔注射纳美芬(NTI)或1mg/kg腹腔注射去甲苄尼地平(NOR-BNI),并未使DEX诱导的口腔面部试验抗伤害感受的ED值产生显著变化。用0.5mg/kg腹腔注射托烷司琼对小鼠进行预处理,显著提高了DEX的ED值。当用5mg/kg腹腔注射L-硝基精氨酸甲酯(L-NAME)或25mg/kg腹腔注射氨基胍或50mg/kg腹腔注射7-硝基吲唑时,可逆转DEX的抗伤害感受作用。

结论

本研究结果表明,在炎症性疼痛小鼠模型中,NO和5-羟色胺途径的激活在DEX的全身抗伤害感受作用中起重要作用。

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