Study on pathogenesis of mice model of coronary heart disease with phlegm-blood stasis syndrome based on PPARγ pathway
10.7501/j.issn.0253-2670.2020.05.025
- Author:
Man FENG
1
Author Information
1. Tianjin University of Traditional Chinese Medicine
- Publication Type:Journal Article
- Keywords:
Ang II;
Coronary heart disease;
ET;
MMP-9;
NF-κB;
Phlegm-blood stasis syndrome;
PPARγ
- From:
Chinese Traditional and Herbal Drugs
2020;51(5):1273-1278
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To explore the pathogenesis of phlegm-blood stasis syndrome in mice model of coronary heart disease based on PPAR gamma pathway. Methods: Healthy SPF C57BL/6J mice were used in the control group and the sham operation group, and ApoE-/-mice were used in the blood stasis group, phlegm turbid group and phlegm-blood stasis group. The phlegm turbid group and the phlegm-blood stasis group were fed with high-fat diet for 12 weeks, and the other groups were fed with normal feed for 12 weeks. At the end of the 8th week, the left anterior descending coronary artery was ligated in the blood stasis group and the phlegm-blood stasis group. The sham operation group was not ligated. The levels of IL-6, ET, Ang II and PPARγ in serum were measured by enzyme linked immunosorbent assay, the levels of PPARγ, ABCA1 and CD36 protein in liver tissue were detected by Western blotting, and the levels of CD40, MMP-9 and NF-κB protein in aorta were detected by immunohistochemistry. Results: Compared with sham operation group, there was no significant change in serum IL-6, the content of serum ET in the group of phlegm and blood stasis was increased significantly (P < 0.01), the content of Ang II in blood stasis group was increased significantly (P < 0.05), the content of serum Ang II in phlegm turbid group and phlegm-blood stasis group was increased significantly (P < 0.01), and the content of PPARγ was decreased. In liver tissue, the expression levels of PPARγ and ABCA1 protein in blood stasis group, phlegm turbid group and phlegm-blood stasis group were decreased significantly (P < 0.01), the expression of CD36 protein was increased. CD40, MMP-9 and NF-κB levels in aorta tissue were increased significantly (P < 0.01). Conclusion: The phlegm-blood stasis syndrome of coronary heart disease can cause more serious atherosclerotic plaque in the course of its onset. Its mechanism may be through activating PPARγ pathway.
