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 investigate the protective effect of hydroxysafflor yellow A (HSYA), a soluble element extracted from Carthamus tinctorius L., on focal cerebral ischemia in rats.</p><p><b>METHODS</b>Focal cerebral ischemia in male Wistar-Kyoto (WKY) rats were induced by permanent middle cerebral artery occlusion (MCAO). Three doses of 1.5, 3.0 and 6.0 mg x kg(-1) of HSYA were administrated to three groups of rats, separately, via sublingular vein injection 30 min after the onset of ischemia. 24 h after ischemia in rats, neurological deficit scores were evaluated and the infarction area of brain was assessed by quantitative image analysis. The in vitro neuroprotective effect of HSYA was tested in cultured fetal cortical neurons exposed to glutamate and sodium cyanide (NaCN).</p><p><b>RESULTS</b>HSYA at doses of 3.0 and 6.0 mg x kg(-1) exerted significant neuroprotective effects on rats with focal cerebral ischemic injury as expressed by neurological deficit scores and reduced the infarct area as compared with saline group, and the potency of HSYA at dose of 6.0 mg x kg(-1) was similar to that of 0.2 mg x kg(-1) of nimodipine. In vitro studies, HSYA significantly inhibited neurons damage induced by exposure to glutamate and NaCN in cultured fetal cortical cells.</p><p><b>CONCLUSION</b>HSYA has potential neuroprotective action against focal cerebral ischemia in rats and cultured rat fetal cortical neurons as well.</p>
Subject(s)
Animals , Male , Rats , Behavior, Animal , Brain , Pathology , Brain Ischemia , Pathology , Carthamus tinctorius , Chemistry , Cells, Cultured , Cerebral Cortex , Cell Biology , Chalcone , Pharmacology , Glutamic Acid , Infarction, Middle Cerebral Artery , L-Lactate Dehydrogenase , Metabolism , Neurons , Cell Biology , Metabolism , Neuroprotective Agents , Pharmacology , Plants, Medicinal , Chemistry , Quinones , Pharmacology , Rats, Inbred WKY , Sodium CyanideABSTRACT
<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>