ABSTRACT
<p><b>OBJECTIVE</b>To observe the protective effects of total flavones of metasequosia (TFM) on cerebral ischemia-reperfusion injury in rats.</p><p><b>METHOD</b>The bilateral vertebral arteries of rats were occluded under anesthesia, and 4-5 h later the carotid arteries of rats in the conscious condition were occluded for 30 min followed by reperfusion for 90 min. The effects of TFM on the contents of water, Na+, Ca2+ in cortex, malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in brain hemispheres, as well as the EEG activities were observed.</p><p><b>RESULT</b>After 30 min ischemia and 90 min reperfusion, the contents of water, Na+ , Ca2+ and MDA were increased, and the SOD activity was reduced with abnormal EEG activity and ischemic injury in the brain tissues. TFM 25-100 mg x kg(-1) ip 30 min before the carotid arteries were occluded, decreased the elevated water, Na+, Ca2+ and MDA contents, increased the SOD activity, reduced the ischemic injury of brain tissue, and promoted the recovery of EEG activities.</p><p><b>CONCLUSION</b>TFM has a protective effect on cerebral ischemia-reperfusion injury in rats.</p>
Subject(s)
Animals , Male , Rats , Brain , Metabolism , Brain Ischemia , Electroencephalography , Flavones , Pharmacology , Neuroprotective Agents , Pharmacology , Plants, Medicinal , Chemistry , Rats, Sprague-Dawley , Reperfusion Injury , Metabolism , Pathology , Cupressaceae , ChemistryABSTRACT
To observe the effects of total flavones of Metasequoia glyptostroboides Hu et Cheng (TFM) on volume-overload cardiac hypertrophy and the expression of c-Fos protein in rat. Methods Volume-overload cardiac hypertrophy of rat was induced by aortocaval shunts. The rats were given ig TFM (400, 40 and 4 mg/kg/d). c-Fos protein in the ventricles were measured by immunocytochemical study. Results TFM at the above dosage decreased heart weight and contents of RNA and protein in the myocardium, inhibited the expression of c-Fos protein in the ventricles. Conclusion TFM can prevent volume-overload cardiac hypertrophy in rats. The inhibitory effects on the expression of c-Fos protein may be its mechanism in the molecular level.