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小剂量阿司匹林对根尖周液中阿司匹林触发的脂氧素、白细胞介素 1β和前列腺素 E2 水平的影响:一项双盲随机临床试验。

The effect of low-dose aspirin on aspirin triggered lipoxin, interleukin 1 beta, and prostaglandin E2 levels in periapical fluid: a double-blind randomized clinical trial.

机构信息

Department of Endodontics, Dental School, Hamadan University of Medical Sciences, Hamadan, Iran.

Department of Endodontics, School of dentistry, Qazvin University of Medical Sciences, Qazvin, Iran.

出版信息

BMC Oral Health. 2023 Jul 31;23(1):530. doi: 10.1186/s12903-023-03243-0.

Abstract

BACKGROUND

The role of pro-resolving mediators in inflammation is a new concern in research. The effect of low-dose aspirin on production of a special kind of these mediators named aspirin triggered lipoxin (ATL) has been studied on different tissues. This randomized clinical trial evaluated the effect of low-dose aspirin on ATL and pro-inflammatory mediators' level in periapical fluid of necrotic teeth with large lesions.

METHODS

Twenty-four patients with necrotic pulp and periapical lesion were randomly assigned to low-dose aspirin and placebo groups. In the first appointment, canals were shaped up to F3 size and #40 K-file and cleaned with 10 milliliters 2.5% sodium hypochlorite and 17% Ethylenediaminetetraacetic acid. Periapical fluid was sampled by a paper cone. The tooth was temporized without any intracanal medication. Tablets were administered for 7 days, then the teeth were re-opened and the sampling were repeated. Interleukin-1 beta (IL-1β), prostaglandin E2 (PGE2) and ATL were analyzed by enzyme-linked immunosorbent assay. Data were analyzed with paired t-test using SPSS statistical software, version 21 (α = 0.05).

RESULTS

A significant reduction in PGE2 and IL-1β was noted in the aspirin-treated group while an increase in ATL was observed (P < 0.001). There was no significant difference in the mediator scores before and after in the placebo-treated group (P > 0.05).

CONCLUSION

Low-dose aspirin can influence the inflammatory process by reducing pro-inflammatory mediators such as PGE2 and IL-1β, as well as increasing the pro-resolving mediators such as ATL.

TRIAL REGISTRATION

IRCT20191211045702N1.

摘要

背景

在炎症研究中,促炎消退介质的作用是一个新的关注点。已经在不同组织中研究了低剂量阿司匹林对一种特殊的这类介质(称为阿司匹林触发的脂氧素(ATL))产生的影响。这项随机临床试验评估了低剂量阿司匹林对大病变坏死牙髓和根尖周液中 ATL 和促炎介质水平的影响。

方法

将 24 名患有坏死牙髓和根尖周病变的患者随机分为低剂量阿司匹林组和安慰剂组。在第一次就诊时,根管被成形至 F3 尺寸和 #40 K 锉,并使用 10 毫升 2.5%次氯酸钠和 17%乙二胺四乙酸进行清洁。通过纸锥抽取根尖周液。牙齿暂封,不使用任何根管内药物。口服片剂 7 天,然后重新打开牙齿并重复取样。采用酶联免疫吸附试验分析白细胞介素-1β(IL-1β)、前列腺素 E2(PGE2)和 ATL。使用 SPSS 统计软件(版本 21,α=0.05)对数据进行配对 t 检验分析。

结果

阿司匹林治疗组 PGE2 和 IL-1β 显著降低,而 ATL 增加(P<0.001)。安慰剂治疗组治疗前后介质评分无显著差异(P>0.05)。

结论

低剂量阿司匹林可通过降低促炎介质(如 PGE2 和 IL-1β),增加促消退介质(如 ATL)来影响炎症过程。

试验注册

IRCT20191211045702N1。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3f1/10388445/356ec5d75060/12903_2023_3243_Fig1_HTML.jpg

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