ABSTRACT
<p><b>OBJECTIVE</b>To study the protective effect of ligusticum chuanxiong phthalides on cerebral ischemia in rats and its related mechanism of action.</p><p><b>METHOD</b>Middle cerebral artery occlusion (MCAO) model, thrombosis formation, platelet aggregation and hemorrheological parameters were measured to evaluate the protective effect of ligusticum chuanxiong phthalides.</p><p><b>RESULT</b>Ligusticum chuanxiong phthalides could markedly decrease the infarct size and behavior deficits score, inhibit the thrombus formation and platelet aggregation, ameliorate hemorrheological parameters with a dose-dependent manner in rats.</p><p><b>CONCLUSION</b>Ligusticum chuanxiong phthalides has protective effects on focal cerebral ischemia in rats, and its mechanism may be relevant to its inhibition of platelet-dependent thrombosis and amelioration of hemorrheological parameters.</p>
Subject(s)
Animals , Male , Rats , Benzofurans , Pharmacology , Blood Viscosity , Brain Ischemia , Blood , Pathology , Dose-Response Relationship, Drug , Hematocrit , Infarction, Middle Cerebral Artery , Blood , Pathology , Ligusticum , Chemistry , Neuroprotective Agents , Pharmacology , Plants, Medicinal , Chemistry , Platelet Aggregation , Rats, Wistar , Venous ThrombosisABSTRACT
<p><b>AIM</b>To study the effects of hydroxysafflor yellow A (HSYA) on the mitochondrial function of cortex mitochondrial during cerebral ischemia in rats.</p><p><b>METHODS</b>Rat focal cerebral ischemia model in rats was established by ligation of middle cerebral central artery. Cortex mitochondria were isolated and prepared for the measurement of membrane fluidity, swelling, respiratory function, activities of mitochondrial respiratory enzymes and superoxide dismutase (SOD), contents of phospholipid, malondial dehyde (MDA) and Ca2+ to evaluate the function of mitochondria.</p><p><b>RESULTS</b>Focal cerebral ischemia resulted in severe neuronal mitochondrial injuries, which could be alleviated by i.v. HSYA (10, 20 mg x kg(-1)), and nimodipine (Nim, 1.0 mg x kg(-1)). The swelling of mitochondria was ameliorated, the decomposability of membrane phospholipid was decreased, the membrane fluidity of mitochondria was increased, HSYA also significantly inhibited the decrease in the activities of respiratory enzymes and SOD of mitochondria, and the increase in MDA and Ca2+ levels caused by cerebral ischemia in rats.</p><p><b>CONCLUSION</b>HSYA showed a protective action against the cortex mitochondrial injuries in rats induced by cerebral ischemia. The mechanisms may be derived from reducing lipid peroxides, inhibiting Ca2+ overload, scavenging free radicals and improving the energy metabolism.</p>