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The antagonism of 6-shogaol in high-glucose-activated NLRP3 inflammasome and consequent calcification of human artery smooth muscle cells

Authors
  • Chen, Te-Chuan1
  • Yen, Chia-Kung2
  • Lu, Ying-Chen2
  • Shi, Chung-Sheng3, 4
  • Hsieh, Rong-Ze3, 4
  • Chang, Shun-Fu4
  • Chen, Cheng-Nan5
  • 1 Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan , Kaohsiung (Taiwan)
  • 2 National Chiayi University, Chiayi, Taiwan , Chiayi (Taiwan)
  • 3 Chang-Gung University, Taoyuan, Taiwan , Taoyuan (Taiwan)
  • 4 Chang Gung Memorial Hospital, Chiayi, Taiwan , Chiayi (Taiwan)
  • 5 National Chiayi University, Chiayi, 600, Taiwan , Chiayi (Taiwan)
Type
Published Article
Journal
Cell & Bioscience
Publisher
Springer (Biomed Central Ltd.)
Publication Date
Jan 09, 2020
Volume
10
Issue
1
Identifiers
DOI: 10.1186/s13578-019-0372-1
Source
Springer Nature
Keywords
License
Green

Abstract

BackgroundVascular calcification is the major reason for high mortality of cardiovascular complications for diabetes. Interleukin (IL)-1β has been implicated in this pathogenesis, but its precise role and clinical evidence have not been clearly identified. Hence, this study was aimed to investigate whether high concentration of glucose (HG), which mimics the hyperglycemia environment, could initiate vascular calcification through NLRP3/IL-1β inflammasome and the underlying mechanism. Recently, 6-shogaol, a major ginger derivate, has been elucidated its pharmaceutic role for various diseases. Therefore, the aims of this study also determined 6-shogaol effect in vascular calcification of HG initiation.ResultHuman artery smooth muscle cells (HASMCs) were used in this study. Glucose concentrations at 5 and 25 mM were defined as normal and HG status, respectively. The results showed that HG could increase the NLRP3, cleaved caspase 1, and pro/mature IL-1β levels to induce the expressions of bone-related matrix proteins and subsequent HASMC calcification. This process was regulated by Akt activation and reactive oxygen species (ROS) production. Moreover, 6-shogaol could inhibit the Akt/ROS signaling and NLRP3/caspase 1/IL-1β inflammasome and hence attenuated HASMC calcification.ConclusionsThis study elucidates the detailed mechanism of HG-initiated HASMC calcification through NLRP3/caspase 1/IL-1β inflammasome and indicates a potential therapeutic role of 6-shogaol in vascular calcification complication of diabetes.

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