The
therapeutic effects of
hydroxysafflor yellow A (HSYA), extracted from Carthamus tinctorius. L, on focal cerebral ischemic injury in rats and its related mechanisms have been investigated. Focal
cerebral ischemia in rats were made by inserting a monofilament
suture into internal carotid artery to block the origin of the middle cerebral artery and administrated by HSYA via sublingular vein injection in doses of 1.5, 3.0, 6.0 mg kg(-1) at 30 min after the onset of
ischemia, in comparison with the potency of
nimodipine at a dose of 0.2 mg kg(-1). Then, 24 h later, the evaluation for neurological deficit scores of the rats were recorded and postmortem
infarct areas determined by quantitative image analysis. At the end of the experiment, blood samples were taken to determine plasma 6-Keto-
PGF1alpha/TXB2 by radioimmunoassays and blood rheological parameters. The effects exerted by HSYA on
thrombosis formation by artery vein by-pass method and
ADP-induced platelet aggregation in vivo and in vitro were investigated, respectively. The results indicated that more than 30% of the area of ischemic cerebrum was observed in the ischemic model group. HSYA dose-dependently improved the neurological deficit scores and reduced the
cerebral infarct area, and HSYA bore a similarity in potency of the
therapeutic effects on focal
cerebral ischemia to
nimodipine. The inhibition rates of
thrombosis formation by HSYA at the designated doses were 20.3%, 43.6% and 54.2%, respectively, compared with saline-treated group. Inhibitory activities of HSYA were observed on
ADP-induced platelets aggregation in a dose-dependent manner, and the maximum inhibitory aggregation rate of HSYA was 41.8%. HSYA provided a suppressive effect on production of TXA2 without significant effect on plasma PGI2 concentrations. Blood rheological parameters were markedly improved by HSYA, such as whole blood viscosity (from 21.71 +/- 4.77 to 11.61 +/- 0.90 mPa.s), plasma viscosity (from 2.73 +/- 0.53 to 1.42 +/- 0.07 mPa.s), deformability (from 0.66 +/- 0.26 to 0.77 +/- 0.33) and aggregation of erythrocyte (from 3.24 +/- 0.41 to 2.57 +/- 0.30), but no significant effect of HSYA on homatocrit was found (from 51.38 +/- 4.68% to 49.91 +/- 2.32%). HSYA appears to be a good potential agent to treat focal
cerebral ischemia, and the underlying mechanisms exerted by HSYA might be involved in its inhibitory effects on
thrombosis formation and platelet aggregation as well as its beneficial action on regulation of PGI2/TXA2 and blood rheological changes in rats.