Research articles
ScienceAsia 51 (2025):ID 2025070 1-10 |doi:
10.2306/scienceasia1513-1874.2025.070
Hydroxysafflor yellow A attenuates oxLDL-induced tissue
factor in monocytes and reduces thrombosis in dyslipidemic
rats
Yangyang Wanga,*, Xinyao Rena, Hui Lib, Peng Wana, Qianchen Wanga, Jingyan Wanga,*, Yingjian Houc,*
ABSTRACT: Safflower, a traditional Chinese herbal medicine, has been approved in China for the treatment of patients
with thrombotic cardiovascular events. However, the exact mechanisms by which this herbal medicine protects against
these diseases remain elusive. Hydroxysafflor yellow A (HSYA) is a major component of Safflower. Tissue factor
(TF) plays a pivotal role in thrombosis formation and propagation. In this study, oxidized low-density lipoprotein
(oxLDL)-challenged monocytic THP-1 cells were pretreated with HSYA alone or in combination with 2-chloro-5-nitro
N-phenylbenzamide (GW9662), a peroxisome proliferator-activated receptor-? (PPAR?) antagonist. Then, TF, PPAR?
and phospho-p38 MAPK levels were assessed by real-time PCR and Western blot. In addition, HSYA or HSYA plus
GW9662 were administered to rats fed a high-fat diet (HFD) for 4 weeks, and TF, PPAR? and phospho-p38 MAPK
levels in peripheral blood mononuclear cells (PBMCs) were evaluated, as well as plasma lipids and thrombus formation
were measured. The results showed that HSYA pretreatment reversed oxLDL-induced TF expression and p38 MAPK
phosphorylation, and promoted PPAR? expression and activity in THP-1 cells. Plasma lipid and oxLDL amounts
were elevated in HFD-fed rats. Although failing to change lipid profile, HSYA reduced TF expression, p38 MAPK
phosphorylation, thrombus formation, and promoted PPAR? expression and activity in dyslipidemic rats. GW9662
abolished the effects of HSYA in monocytes. The results indicated that HSYA attenuates oxLDL-induced TF expression
in monocytes, and reduces arterial and venous thrombus formation in dyslipidemic rats. These effects of HSYA are
likely dependent on PPAR? upregulation and subsequent p38 MAPK inhibition.
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| a |
Affiliated Hospital of Hebei University, Baoding, Hebei 071000 China |
| b |
Xiong?an Xuanwu Hospital, Baoding, Hebei 071000 China |
| c |
Hebei University, Baoding, Hebei 071000 China |
* Corresponding author, E-mail: wangyangyang2019@126.com, hdfywjy@sina.com, houyingjian@126.com
Received 10 Jun 2024, Accepted 9 Jun 2025
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