Mechanism of Gegen Qinliantang against Vulnerable Plaque of Atherosclerosis: Based on Macrophage Pyroptosis Mediated by NF-κB/NLRP3/Caspase-1 Pathway / 中国实验方剂学杂志
Chinese Journal of Experimental Traditional Medical Formulae
; (24): 70-78, 2022.
Article
in Zh
| WPRIM
| ID: wpr-940622
Responsible library:
WPRO
ABSTRACT
ObjectiveTo explore the effect of Gegen Qinliantang (GQL) on vulnerable plaque of atherosclerosis based on the macrophage pyroptosis mediated by nuclear factor (NF)-κB/NOD-like receptor protein 3 (NLRP3)/cysteine-aspartic acid protease (Caspase)-1 pathway. MethodA total of 12 normal C57BL/6CNC mice were used as the control group, and 60 ApoE-/- mice of the same line were randomized into 5 groups: model group, low-dose, medium-dose, and high-dose GQL groups (GQL-D, GQL-Z, GQL-G groups, respectively), and western medicine group. The control group and model group were given (ig) equal volume sterile distilled, and GQL-D, GQL-Z, GQL-G and western medicine groups received (ig) corresponding concentration of drugs for 8 weeks. Aortic plaques were observed based on hematoxylin and eosin (HE) staining. Serum levels of interleukin (IL)-1β and IL-18 were detected by enzyme-linked immunosorbent assay (ELISA), protein levels of macrophage mannose receptor (CD206)/apoptosis-associated speck-like protein containing a CARD (ASC) and CD206/NLRP3 by double-labeling immunofluorescence, and C-terminal gasdermin D (GSDMD), N-terminal GSDMD, NLRP3, pro-cysteinyl aspartate specific proteinase 1 (pro-Caspase-1) and NF-κB p65 by Western blot. ResultCompared with the control group, model group demonstrated serious pathological changes, rise of the levels of serum IL-1β and IL-18 and tissue ASC, NLRP3, C-terminal GSDMD, N-terminal GSDMD, pro-Caspase-1, and NF-κB p65, and decrease of CD206 level (P<0.05). As compared with model group, the administration groups showed alleviation of the lesions in aortic wall, decrease in levels of serum IL-1β and IL-18 and tissue ASC, NLRP3, C-terminal GSDMD, N-terminal GSDMD, pro-Caspase-1, and NF-κB p65, and rise of CD206 level, with significant difference between some groups (P<0.05). ConclusionGegen Qinliantang alleviates vulnerable plaque of atherosclerosis by regulating NF-κB/NLRP3/Caspase-1 pathway and further relieving macrophage pyroptosis.
Full text:
1
Database:
WPRIM
Type of study:
Clinical_trials
/
Prognostic_studies
Language:
Zh
Journal:
Chinese Journal of Experimental Traditional Medical Formulae
Year:
2022
Document type:
Article