Suppr超能文献

没食子酸肉桂酯通过下调 NF-κb 介导的炎症反应对离心运动诱导的骨骼肌损伤的改善作用。

Ameliorative effects of caffeic acid phenethyl ester on an eccentric exercise-induced skeletal muscle injury by down-regulating NF-κb mediated inflammation.

机构信息

Department of Chinese Martial Arts, Chinese Culture University, Taipei, Taiwan, ROC.

出版信息

Pharmacology. 2013;91(3-4):219-28. doi: 10.1159/000348412. Epub 2013 Apr 3.

Abstract

BACKGROUND AND PURPOSE

Caffeic acid phenethyl ester (CAPE), a phenolic compound isolated from propolis, displays a variety of biological activities. The aim is to examine the protective effect and mechanisms of CAPE on an eccentric exercise-induced muscle injury model.

EXPERIMENTAL APPROACH

An intermittent downhill eccentric exercise protocol was used. The oxidative tissue injury and expression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), interleukin-1β (IL-1β), monocyte chemotactic protein-1 (MCP-1), and activation of nuclear factor-κB (NF-κB) were examined. CAPE was applied in a dose of 5 and 10 mg/kg/day, p.o.

KEY RESULTS

The eccentric exercise induced remarkable skeletal muscle damage uncovered by a dramatic elevation of creatine kinase in the serum and severe degenerative myopathy. These pathophysiological changes were accompanied by an upregulation of the inflammatory responses including protein nitrotyrosylation, poly-ADP-ribose-polymerase (PARP) upregulation, lipid peroxidation as measured by malondialdehyde (MDA) formation, and leukocyte infiltration as measured by myeloperoxidase (MPO). The inflammatory responses primarily resulted from enhanced expression of COX2, iNOS, and production of IL-1β and MCP-1, possibly through activation of NF-κB. All these pathological changes were suppressed by treatment of CAPE.

CONCLUSIONS AND IMPLICATIONS

Our results indicate that CAPE exhibits protective effects against eccentric exercise-induced skeletal muscle damage in rats by blocking the NF-κB-dependent activation of the inflammatory responses.

摘要

背景与目的

咖啡酸苯乙酯(CAPE)是从蜂胶中分离出的一种酚类化合物,具有多种生物活性。本研究旨在探讨 CAPE 对离心运动诱导肌肉损伤模型的保护作用及其机制。

实验方法

采用间歇性下坡离心运动方案。检测氧化组织损伤和环氧化酶-2(COX-2)、诱导型一氧化氮合酶(iNOS)、白细胞介素-1β(IL-1β)、单核细胞趋化蛋白-1(MCP-1)的表达以及核因子-κB(NF-κB)的激活。CAPE 以 5 和 10 mg/kg/天的剂量灌胃给药。

主要结果

离心运动导致血清肌酸激酶显著升高和严重退行性肌病,从而引起明显的骨骼肌损伤。这些病理生理变化伴随着炎症反应的上调,包括蛋白硝基化、多聚 ADP-核糖聚合酶(PARP)上调、丙二醛(MDA)形成所测脂质过氧化以及髓过氧化物酶(MPO)所测白细胞浸润。炎症反应主要是由于 COX2、iNOS 的表达增强以及 IL-1β和 MCP-1 的产生所致,可能通过 NF-κB 的激活。所有这些病理变化均被 CAPE 治疗抑制。

结论和意义

我们的研究结果表明,CAPE 通过阻断 NF-κB 依赖性炎症反应的激活,对大鼠离心运动诱导的骨骼肌损伤具有保护作用。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验