echinacoside and Infarction--Middle-Cerebral-Artery

To evaluate the effect of echinacoside (ECH) on cognitive dysfunction in post cerebral stroke model rats.. The post stroke cognitive impairment rat model was created by occlusion of the transient middle cerebral artery (MCAO). The rats were randomly divided into 3 groups by a random number table: the sham group (sham operation), the MCAO group (received operation for focal cerebral ischemia), and the ECH group (received operation for focal cerebral ischemia and ECH 50 mg/kg per day), with 6 rats in each group. The infarct volume and spatial learning were evaluated by triphenyl tetrazolium chloride staining and Morris water maze. The expression of α7nAChR in the hippocampus was detected by immunohistochemistry. The contents of acetylcholine (ACh), malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), activities of choline acetyltransferase (ChAT), acetylcholinesterase (AChE), and catalase (CAT) were evaluated by enzyme linked immunosorbent assay. The neural apoptosis and autophagy were determined by TUNEL staining and LC3 staining, respectively.. ECH significantly lessened the brain infarct volume and ameliorated neurological deficit in infarct volume and water content (both P<0.01). Compared with MCAO rats, administration of ECH revealed shorter escape latency and long retention time at 7, 14 and 28 days (all P<0.01), increased the α7nAChR protein expression, ACh content, and ChAT activity, and decreased AChE activity in MCAO rats (all P<0.01). ECH significantly decreased MDA content and increased the GSH content, SOD, and CAT activities compared with MCAO rats (all P<0.05). ECH suppressed neuronal apoptosis by reducing TUNEL-positive cells and also enhanced autophagy in MCAO rats (all P<0.01).. ECH treatment helped improve cognitive impairment by attenuating neurological damage and enhancing autophagy in MCAO rats.

Topics: Acetylcholinesterase; alpha7 Nicotinic Acetylcholine Receptor; Animals; Autophagy; Brain Ischemia; Cerebral Infarction; Cognitive Dysfunction; Glutathione; Glycosides; Infarction, Middle Cerebral Artery; Neuroprotective Agents; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Stroke; Superoxide Dismutase

Topics: Animals; beta Catenin; Casein Kinase II; Disease Models, Animal; Gene Expression Regulation; Gene Knockdown Techniques; Glycosides; GTP Phosphohydrolases; Humans; Infarction, Middle Cerebral Artery; Ischemic Stroke; Lymphoid Enhancer-Binding Factor 1; Mice; Mitochondrial Dynamics; Multiprotein Complexes; Neuroprotection; Nuclear Proteins; T Cell Transcription Factor 1; Transcription Factors; Transcription, Genetic

To investigate the effects of echinacoside on the extracellular striatal levels of norepinephrine (NE), dopamine (DA), homovanillic acid (HVA), 3, 4-dihydroxyphenylethanoid acid (DOPAC), 5-hydroxyindoleacetic acid (HIAA), and 5-hydroxytryptamine(5-HT) in middle cerebral artery occlusion (MCAO rats.. The middle cerebral artery was occluded in male Sprague-Dawley rats. Three days later microdialysis probes were placed into the right striatum of MCAO rat brains and the brains were perfused with Ringer's solution at a rate of 1.5 microL/min. Cerebral microdialysates were collected every 30 minutes from awake and freely moving rats before assaying for NE, DA, HVA, DOPAC, HIAA, and 5-HT levels by reverse phase HPLC with electrochemistry.. Three days after MCAO, the extracellular striatal levels of NE, DA, DOPAC, HIAA, HVA, and 5-HT of the MCAO rats increased significantly (at least P < 0.05 vs. control). However, simultaneous treatment with echinacoside (30.0 or 15.0 mg/kg) attenuated these increases (at least P < 0.05 vs. non-treated model rats).. These results imply that echinacoside may protect striatal dopa minergic neurons from the injury induced by MCAO and may help prevent and treat cerebral ischemic diseases.

Topics: Animals; Glycosides; Infarction, Middle Cerebral Artery; Male; Rats; Rats, Sprague-Dawley