AIM: To investigate the effect of erigeron on intercellular adhesion molecule-1 (ICAM-1) and mRNA expression during cerebral ischemia/reperfusion. METHODS: The rat models of middle cerebral artery (MCA) focal cerebral ischemic reperfusion were established with the suture method in the study. The ICAM-1 mRNA and protein expression were measured by RT-PCR and immunohistochemistry techniques, respectively. RESULTS: By down-regulating the expression of ICAM-1 protein and mRNA and alleviating inflammation in cerebral ischemic region, erigeron exerted a protective effect in cerebral ischemia and reperfusion. CONCLUSION: The results suggest that erigeron protects the brain against cerebral ischemia and reperfusion injury via inhibiting ICAM-1 expression. [

AIM To compare the effect of Piper Futokadsura Neoligans with Ginkgolides, a platelet activiting factor receptor antagonist, on cerebral ischemic area,region cerebral blood flow(rCBF) and neuroligic function deficits following focal cerebral ischemia/reperfusion in rats. METHODS The middle cerebral artery (MCA) focal cerebral ischemia and reperfusion rat models were used. The cerebral ischemic area, rCBF and neural function deficits were measured by TTC staining,hydyogen clearance and neurologic function scoring, respectively. RESULTS A significant reduction in infarct volume were found in the Piper Futokadsura Neoligans treated group as well as in the Ginkgolides treated group compared with the control group.Furthermore, Piper Futokadsura Neoligans induced significant amelioration of the rCBF decrease and neurologic dysfunction following focal cerebral ischemia and reperfusion in rats. CONCLUSION Both Piper Futokadsura Neoligans and Ginkgolides have remarkable brain protective effects.

OBJECTIVETo investigate the effects of antisense glutamic acid decarboxylase (GAD(67)) oligodeoxynucleo-tide (ODN) on behavior, seizure threshold and EEG of hippocampus in the epileptic rats induced by pentylenetetrazol (PTZ).

METHODSA model of chronic epilepsy in rats was established by PTZ. The inhibition of GAD(67) mRNA expression in hippocampus was selectively induced by antisense oligodeoxynucleotide of GAD(67). The effect of antisense GAD(67) ODN on behavior, seizure threshold and EEG recording of kindled rats was examined.

RESULTSAntisense GAD(67) ODN could inhibit the expression of GAD(67) mRNA and the concentration of GABA. It also could significantly shorten the latencies of seizure and increase the level of seizure and the frequency of epileptiform discharges.

CONCLUSIONThe gene of GAD(67) may be an anti-seizure gene, which might inhibit epileptiform discharge. The treatment of epilepsy by GAD(67) gene will have a bright future.

Animals ; Electroencephalography ; Epilepsy ; chemically induced ; physiopathology ; Glutamate Decarboxylase ; genetics ; pharmacology ; Hippocampus ; physiopathology ; Isoenzymes ; genetics ; pharmacology ; Kindling, Neurologic ; Male ; Oligonucleotides, Antisense ; pharmacology ; Pentylenetetrazole ; Rats ; gamma-Aminobutyric Acid ; analysis

OBJECTIVETo study whether recombinant adeno-associated virus (rAAV) mediated foreign gene, LacZ, could pass the blood brain barrier by intra-carotid artery delivery and express in vivo in ischemic brain of the focal embolic stroke rats to investigate a possibility of delivering foreign gene through carotid artery to treat acute ischemic stroke.

METHODSThe carotid artery territory in 41 rats was embolized with or without arterial-like fibrin rich clots to make a model of focal embolic stroke rat. rAAV containing LacZ gene (rAAV-LacZ) was constructed in 293 cells by calcium phosphate cotransfection. The rats were assigned to one of the following treatments: 1 control (without embolism) groups, including PBS treated (n = 6), pLacZ treated (n = 6 ) and rAAV-LacZ treated (n = 6): 2 embolic groups, including embolism + PBS (n =7),embolism + pLacZ (n = 8) and embolism + rAAV-LacZ (n = 8). Brains were cryosectioned and kappa-Gal stain was performed at 2, 4, and 8 weeks, respectively, after transfection, and then infarct volume was measured and the percentage of LacZ staining-positive cells was calculated.

RESULTSIn all the control groups and embolism + PBS treated animal, no kappa-Gal staining-positive cells were found, but in embolism + pLacZ (n = 8) and embolism+rAAV-LacZ groups a lot of kappa-Gal staining-positive cells were found. The expression cells were in the tissues around the infarction. The gene expression persisted only nearly four weeks in embolic group with pLacZ. In the embolic group with rAAV-LacZ the expression was very stable during the experiment course (eight weeks) and the percentage of the expressed cells was significantly higher than that of its contralateral areas at the same time points, respectively.

CONCLUSIONSThe plasmid vector and rAAV could enter the brain through the ischemia-damaged blood barrier and foreign gene can be expressed in brain. The positive gene expression is mainly in the peripheral areas of the infarction. rAAV as a permanent expression vector may ultimately be used for gene therapy of human ischemia cerebravascular diseases.

Animals ; Blood-Brain Barrier ; Brain ; virology ; Carotid Arteries ; Dependovirus ; genetics ; Genetic Therapy ; Genetic Vectors ; Intracranial Embolism ; therapy ; Male ; Rats ; Rats, Sprague-Dawley ; Stroke ; therapy