Echinacoside Alleviates Cognitive Impairment in Cerebral Ischemia Rats through α 7nAChR-Induced Autophagy / 中国结合医学杂志

OBJECTIVES@#To evaluate the effect of echinacoside (ECH) on cognitive dysfunction in post cerebral stroke model rats.@*METHODS@#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.@*RESULTS@#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).@*CONCLUSION@#ECH treatment helped improve cognitive impairment by attenuating neurological damage and enhancing autophagy in MCAO rats.

Cholinergic activity related to cardiovascular regulation in rostral ventrolateral medulla of spontaneously hypertensive rats

The hyperactivity of cholinergic system in the RVLM of spontaneously hypertensive rats (SHR) may contribute to the sustained elevation of blood pressure. However, the hyperactivity mechanisms of cholinergic system are controversial. Thus, to clarify the mechanisms of cholinergic hyperactivity in RVLM of the SHR, we studied the activities of enzymes that participate in the biosynthesis and degradation of acetylcholine (ACh) and the density of muscarinic receptors in RVLM of the 14- to 18-week-old SHR and age-marched Wistar Kyoto rats (WKY). Choline acetyltransferase activity was far greater in RVLM of SHR than that of WKY. (3H)ACh release from RVLM was also greater in SHR than in WKY. Acetylcholinesterase activity and (3H)NMS binding of RVLM slice of SHR were not significantly different from that of WKY. These results suggest that the enhanced cholinergic mechanisms in the RVLM of SHR is due to the enhanced presynaptic cholinergic tone rather than the altered postsynaptic mechanisms.

A TOXICOLOGICAL STUDY ON LETHAL EFFECTS OF MONOCROTOPHO / 西安交通大学学报(医学版)

The relation ship between lethal effects and the distribution of monocrotopho contents in the body of mice has been showed by using tracer determination of radioisotope. The authors also observed the difference of degree of inhibited cholinergic activity in blood and brain of mice to which monocrotopho was given orally in different lethal dose. The results showed that there was a close relatiom between the death of monocrotopho acute poison and toxicant contents in brain. At the same time, wealso found there was no significant difference between the degree of inhibited cholinergic activity in blood and brain of survival mice to which monocrotopho was given orally in LD_(50) and dead mice in same dose as well as in excess lethal dose. This paper deals with the toxicological mechanism of the death of monocrotopho poison.