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黄连素通过抑制PI3K/AKT信号通路的激活减轻心肌缺血再灌注损伤。

Berberine attenuates myocardial ischemia reperfusion injury by suppressing the activation of PI3K/AKT signaling.

作者信息

Qin-Wei Zhu, Yong-Guang L I

机构信息

Department of Emergency, Weifang Hospital of Traditional Chinese Medicine, Weifang, Shandong 261041, P.R. China.

Department of Emergency, Weifang Hospital of Traditional Chinese Medicine, Weifang, Shandong 261041, P.R. China; Department of Emergency, Weifang People's Hospital, Weifang, Shandong 261041, P.R. China.

出版信息

Exp Ther Med. 2016 Mar;11(3):978-984. doi: 10.3892/etm.2016.3018. Epub 2016 Jan 22.

Abstract

Berberine (BBR), an isoquinoline alkaloid originally isolated from the Chinese herb (Huanglian), exhibits anti-inflammatory and immunosuppressive properties. Since myocardial ischemia/reperfusion (I/R) injury is associated with an excessive immune response, the current study was conducted to investigate the impact of BBR on myocardial I/R injury, a common disorder in clinical settings. Preconditioning of Sprague-Dawley rats with BBR (100 mg/kg/day, by gavage) for 14 days prior to the induction of I/R significantly attenuated myocardial I/R injury as manifested by a reduction in the incidence of ventricular arrhythmia and the amelioration of myocardial histological changes. These effects were found to be associated with the suppression of the phosphoinositide 3-kinase/AKT signaling pathway and the subsequent reduction of the expression of interleukin (IL)-6, IL-1β, and tumor necrosis factor-α in the serum and myocardial tissue. These results indicate that BBR has the potential be an effective alternative therapy for the prevention and treatment of myocardial I/R injury in clinical practice.

摘要

小檗碱(BBR)是一种最初从中药(黄连)中分离出来的异喹啉生物碱,具有抗炎和免疫抑制特性。由于心肌缺血/再灌注(I/R)损伤与过度的免疫反应有关,因此进行了本研究以探讨BBR对心肌I/R损伤的影响,心肌I/R损伤是临床常见疾病。在诱导I/R前14天,用BBR(100mg/kg/天,经口灌胃)对Sprague-Dawley大鼠进行预处理,可显著减轻心肌I/R损伤,表现为室性心律失常发生率降低和心肌组织学变化改善。发现这些作用与磷酸肌醇3-激酶/AKT信号通路的抑制以及随后血清和心肌组织中白细胞介素(IL)-6、IL-1β和肿瘤坏死因子-α表达的降低有关。这些结果表明,BBR有可能成为临床实践中预防和治疗心肌I/R损伤的有效替代疗法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/027f/4774358/7bdc092e2ccb/etm-11-03-0978-g00.jpg

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