ReferenceID 1064
The antagonism of 6-shogaol in high-glucose-activated NLRP3 inflammasome and consequent calcification of human artery smooth muscle cells
Cell Biosci
Background: Vascular calcification is the major reason for high mortality of cardiovascular complications for diabetes. Interleukin (IL)-1beta has been implicated in this pathogenesis, but its precise role and clinical e
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- Reference Id
- 1064
- Evidence Id
- 17654
- Core Evidence Id
- 17654
- Source Reference Id
- 2110
- Herb2 Reference Id
- HBREF002907
- Subject Paper Key
- HBIN012818_31938471
- Pubmed Id
- 31938471
- Doi
- 10.1186/s13578-019-0372-1
- Paper Title
- The antagonism of 6-shogaol in high-glucose-activated NLRP3 inflammasome and consequent calcification of human artery smooth muscle cells
- Paper Abstract
- Background: Vascular calcification is the major reason for high mortality of cardiovascular complications for diabetes. Interleukin (IL)-1beta 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-1beta 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. Result: Human 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-1beta 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-1beta inflammasome and hence attenuated HASMC calcification. Conclusions: This study elucidates the detailed mechanism of HG-initiated HASMC calcification through NLRP3/caspase 1/IL-1beta inflammasome and indicates a potential therapeutic role of 6-shogaol in vascular calcification complication of diabetes.
- Journal
- Cell Biosci
- Publish Year
- 2020
- Experiment Subject
- human; ginger
- Experiment Type
- Cell Experiment
- Phenotype Related
- Cardiovascular Complications; Hasmc Calcification; Vascular Calcification; Hyperglycemia; Diabetes
- Paper Title Cn
- Paper Title En
- The antagonism of 6-shogaol in high-glucose-activated NLRP3 inflammasome and consequent calcification of human artery smooth muscle cells
- Bilingual Status
- semi_complete