Research progress on mechanism of Carthamus tinctorius in ischemic stroke therapy.
10.19540/j.cnki.cjcmm.20220217.701
- Author:
Jun-Ren CHEN
1
;
Xiao-Fang XIE
1
;
Xiao-Yu CAO
1
;
Gang-Min LI
1
;
Yan-Peng YIN
1
;
Cheng PENG
1
Author Information
1. State Key Laboratory of Southwestern Chinese Medicine Resources, School of Pharmacy,Chengdu University of Traditional Chinese Medicine Chengdu 611137,China.
- Publication Type:Journal Article
- Keywords:
Carthamus tinctorius;
hydroxysafflor yellow A;
ischemic stroke;
research progress
- MeSH:
Carthamus tinctorius/chemistry*;
Chalcone/therapeutic use*;
Cyclooxygenase 2/metabolism*;
Cytokines/metabolism*;
Flavonoids/therapeutic use*;
Glycogen Synthase Kinase 3 beta/metabolism*;
Humans;
Ischemic Stroke/drug therapy*;
Janus Kinase 2/metabolism*;
Mitogen-Activated Protein Kinases/metabolism*;
NF-kappa B/metabolism*;
NLR Family, Pyrin Domain-Containing 3 Protein/metabolism*;
Nitric Oxide/metabolism*;
Nitric Oxide Synthase Type II/metabolism*;
Phosphatidylinositol 3-Kinase/metabolism*;
Phosphatidylinositol 3-Kinases/metabolism*;
Prostaglandin D2;
Proto-Oncogene Proteins c-akt/metabolism*;
Quinones/pharmacology*
- From:
China Journal of Chinese Materia Medica
2022;47(17):4574-4582
- CountryChina
- Language:Chinese
-
Abstract:
Carthamus tinctorius is proved potent in treating ischemic stroke. Flavonoids, such as safflower yellow, hydroxysafflor yellow A(HSYA), nicotiflorin, safflower yellow B, and kaempferol-3-O-rutinoside, are the main substance basis of C. tinctorius in the treatment of ischemic stroke, and HSYA is the research hotspot. Current studies have shown that C. tinctorius can prevent and treat ischemic stroke by reducing inflammation, oxidative stress, and endoplasmic reticulum stress, inhibiting neuronal apoptosis and platelet aggregation, as well as increasing blood flow. C. tinctorius can regulate the pathways including nuclear factor(NF)-κB, mitogen-activated protein kinase(MAPK), signal transducer and activator of transcription protein 3(STAT3), and NF-κB/NLR family pyrin domain containing 3(NLRP3), and inhibit the activation of cyclooxygenase-2(COX-2)/prostaglandin D2/D prostanoid receptor pathway to alleviate the inflammatory development during ischemic stroke. Additionally, C. tinctorius can relieve oxidative stress injury by inhibiting oxidation and nitrification, regulating free radicals, and mediating nitric oxide(NO)/inducible nitric oxide synthase(iNOS) signals. Furthermore, mediating the activation of Janus kinase 2(JAK2)/STAT3/suppressor of cytokine signaling 3(SOCS3) signaling pathway and phosphoinositide 3-kinase(PI3 K)/protein kinase B(Akt)/glycogen synthase kinase-3β(GSK3β) signaling pathway and regulating the release of matrix metalloproteinase(MMP) inhibitor/MMP are main ways that C. tinctorius inhibits neuronal apoptosis. In addition, C. tinctorius exerts the therapeutic effect on ischemic stroke by regulating autophagy and endoplasmic reticulum stress. The present study reviewed the molecular mechanisms of C. tinctorius in the treatment of ischemic stroke to provide references for the clinical application of C. tinctorius.
