Ropivacaine Prevents the Activation of the NLRP3 Inflammasome Caused by High Glucose in HUVECs
Author(s) -
Xin Huang,
Jingyan Jiang,
Lijun Huang,
Qiusheng Ren,
Xiang Gao,
Shenghui Yu
Publication year - 2020
Publication title -
acs omega
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.779
H-Index - 40
ISSN - 2470-1343
DOI - 10.1021/acsomega.0c03143
Subject(s) - ropivacaine , inflammasome , oxidative stress , inflammation , umbilical vein , sirtuin 1 , medicine , gene knockdown , pathogenesis , pharmacology , diabetes mellitus , chemistry , immunology , endocrinology , apoptosis , downregulation and upregulation , biochemistry , in vitro , gene
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.
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