Based on "intestinal flora-inflammation" pathway to investigate effect and mechanism of Danlou Tablet on atherosclerosis of ApoE-/- mice
10.7501/j.issn.0253-2670.2020.09.026
- VernacularTitle: 基于"肠道菌群-炎症"通路探讨丹蒌片防治ApoE-/-小鼠动脉粥样硬化的作用及机制
- Author:
Ying-Xin SUN
1
Author Information
1. Department of Pathology, Tianjin University of Traditional Chinese Medicine
- Publication Type:Journal Article
- Keywords:
ApoE-/- mice;
Atherosclerosis;
Danlou Tablet;
Inflammation;
Intestinal flora
- From:
Chinese Traditional and Herbal Drugs
2020;51(9):2492-2500
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the efficacy and mechanism of Danlou Tablet against atherosclerosis model of ApoE-/- mice fed with high fat diet. Methods: C57BL/6J mice were used as controls and ApoE-/- mice were randomly divided into two groups after 24 weeks of high fat feeding, including the model group received saline and the treatment group received Danlou Tablet. Animals were executed after 8 weeks of treatment and serum was collected to measure blood lipids; Plaque formation in the aorta was observed by red O and HE staining; 16 S rRNA sequencing was used to analyze changes in intestinal flora, and GC-MS test for detection fecal SCFAs content, ELISA for the determination of serum LPS, and real time PCR for detection of mRNA expression. Results: Compared with the control group, the blood lipid levels were increased; intestinal flora was imbalance with increased harmful bacteria and reduced beneficial bacteria; The level of serum LPS and inflammation around the aorta were increased in the model group. Compared with the model group, the contents of TG, TC, LDL-C and the plaque area of Danlou Tablet group were decreased (P < 0.01); Danlou Tablet group can regulate intestinal flora, thus effectively reducing serum LPS and inflammatory factors TNF-α, ICAM-1 and IL-1β levels around the aorta (P < 0.01). Conclusion: Danlou Tablet exerts an anti-atherosclerosis action with favorable efficacy through restructing the intestinal flora stucture, inhibiting endotoxin releasing and constraining the inflammatory response induced by dysbacteriosis.
