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罗哌卡因可预防高糖诱导的人脐静脉内皮细胞中NLRP3炎性小体的激活。

Ropivacaine Prevents the Activation of the NLRP3 Inflammasome Caused by High Glucose in HUVECs.

作者信息

Huang Xin, Jiang Jingyan, Huang Lijun, Ren Qiusheng, Gao Xiang, Yu Shenghui

机构信息

Department of Anesthesiology, The Affiliated People's Hospital of Ningbo University, No. 251, Baizhang East Road, Yinzhou, Ningbo 315040, China.

出版信息

ACS Omega. 2020 Sep 3;5(36):23413-23419. doi: 10.1021/acsomega.0c03143. eCollection 2020 Sep 15.

Abstract

Endothelial dysfunction caused by high glucose is recognized as an important event in the pathogenesis of diabetes-related vascular complications. Ropivacaine is considered to have the best safety profile among the commonly used amide local anesthetics, but the extent of its actions remains incompletely understood. Here, we used human umbilical vein endothelial cells exposed to high glucose to explore the effects of ropivacaine on oxidative stress and markers of inflammation. Ropivacaine treatment exerted significant beneficial effects by rescuing oxidative stress and downregulating interleukin (IL)-1β and IL-18. We also found that ropivacaine could inhibit the secretion of the high-mobility group box 1 protein and improve cell viability. Importantly, sirtuin-1 (SIRT1) knockdown experiments show that the inhibitory effects of ropivacaine against NLRP3 inflammasome activation are dependent on SIRT1. Taken together, these results demonstrate the potential of ropivacaine as a promising therapy against diabetic endothelial dysfunction.

摘要

高糖引起的内皮功能障碍被认为是糖尿病相关血管并发症发病机制中的一个重要事件。在常用的酰胺类局部麻醉剂中,罗哌卡因被认为具有最佳的安全性,但对其作用程度仍不完全清楚。在此,我们使用暴露于高糖环境的人脐静脉内皮细胞来探究罗哌卡因对氧化应激和炎症标志物的影响。罗哌卡因治疗通过减轻氧化应激和下调白细胞介素(IL)-1β及IL-18发挥了显著的有益作用。我们还发现罗哌卡因能够抑制高迁移率族蛋白B1的分泌并提高细胞活力。重要的是,沉默沉默信息调节因子1(SIRT1)的实验表明,罗哌卡因对NLRP3炎性小体激活的抑制作用依赖于SIRT1。综上所述,这些结果证明了罗哌卡因作为治疗糖尿病性内皮功能障碍的一种有前景疗法的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c58/7496028/e797a2baca8f/ao0c03143_0002.jpg

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