Network pharmacology-based study of the mechanism of Ginkgo biloba extract (GBE) in the treatment of atherosclerosis by activating PPARγ
10.11665/j.issn.1000-5048.2024032301
- VernacularTitle:Network pharmacology-based study of the mechanism of Ginkgo biloba extract (GBE) in the treatment of atherosclerosis by activating PPARγ
- Author:
Ziyuan WANG
1
,
2
;
Hui TAO
;
Yingxue XIAO
;
Zhiqi YIN
Author Information
1. 中国药科大学中药学院中药制药系, 南京 211198
2. 中国药科大学中药学院天然药物化学系, 南京 211198
- Publication Type:Journal Article
- Keywords:
Ginkgo biloba extract;
atherosclerosis;
foam cell;
PPARγ
- From:
Journal of China Pharmaceutical University
2025;56(2):225-235
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the effect of Ginkgo biloba extract (GBE) on lipids accumulation and the progression of atherosclerosis(AS), ApoE-/- mice fed with HFD were injected i.g. with two different doses of GBE (GBE-L 50 mg/(kg·d) or GBE-H 150 mg/(kg·d)) for 9 weeks. The core targets and potential mechanisms of GBE therapy for AS were investigated using network pharmacological target prediction. Subsequently, oxidized low-density lipoprotein (ox-LDL)-induced THP-1 was used to investigate the effect of GBE on foam cell formation through oil red staining and Dil-oxLDL fluorescent staining. The mRNA alterations in cholesterol uptake and efflux receptors were detected by real-time quantitative PCR. Finally, the impact of GBE on the expression of PPARγ as the core target was assessed through Western blot and immunofluorescence. It was found that GBE improved serum lipid profile, reduced necrotic cores and lipid deposition in aortic root plaques, and decreased the level of inflammatory factors in serum of ApoE-/- mice. Moreover, GBE treatment reduced the level of intracellular lipid accumulation and inhibited cholesterol uptake and efflux to alleviate foam cell formation. GBE activated PPARγ to enhance ABCA1/ABCG1-induced cholesterol efflux in THP-1. These results suggest that GBE can suppress lipid accumulation and alleviate foam cell formation by activating PPARγ pathway.
