Inhibitory effects of Qushuanling Capsule () on thrombus formation and platelet aggregation in rats.
- Author:
Jie XUE
1
;
Ke-Ping ZHANG
;
Lu-Jia ZHU
;
Mei-Lin XIE
;
Hong-Quan ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: 6-Ketoprostaglandin F1 alpha; blood; Adenosine Diphosphate; pharmacology; Animals; Aorta; drug effects; metabolism; pathology; Cerebral Infarction; blood; drug therapy; pathology; Drugs, Chinese Herbal; pharmacology; therapeutic use; Male; Middle Cerebral Artery; drug effects; pathology; Platelet Aggregation; drug effects; Rats; Rats, Sprague-Dawley; Thrombosis; drug therapy; pathology; Thromboxane B2; blood; Venous Thrombosis; drug therapy; pathology
- From: Chinese journal of integrative medicine 2013;19(2):137-142
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the effects of Qushuanling Capsule ( QSLC) on thrombus formation and platelet aggregation in rats.
METHODSArteriovenous bypass, venous thrombosis, and middle cerebral artery thrombosis models were used in rats to investigate the anti-thrombotic effects of QSLC, a compound of nine Chinese herbs. The platelet aggregation induced by adenosine diphosphate (ADP), thrombin or arachidonic acid (AA), as well as the contents of thromboxane B(2) (TXB(2)) and 6-keto-prostaglandin F1α (6-keto-PGF1α) in rat plasma and aortic walls, were determined to investigate the possible mechanisms of the anti-thrombotic effects of QSLC.
RESULTSAfter oral administration with QSLC for 7 days, arteriovenous bypass thrombosis was obviously suppressed compared with the model group, venous thrombosis was also obviously suppressed, rat behaviors were obviously improved, and brain infarct size as well as water content were also reduced. The platelet aggregation induced by ADP or thrombin was inhibited by QSLC, but the drug had no effect on AA-induced platelet aggregation and content of TXB(2) and 6-keto-PGF1α in plasma and the aortic wall.
CONCLUSIONThese results suggest that QSLC can be used in the prevention and treatment of thrombotic diseases, and that its mechanism of action may be related to inhibition of platelet aggregation.
