Objective To investigate the effects of the exercise training on the cognitive function ,choline acetyltransferase (ChAT) activity and acetylcholinesterase (AchE) activity in stroke prone spontaneously hypertensive rat (SHR/SP) vascular de-mentia model .Methods 30 male SHR/SP rats were randomly divided into sham operation group ,model group and exercise group (n=10) .The VD model was established by the fractional ligation of bilateral carotid artery (2-VO) .The sham operation group and the model group were given the normal feeding without intervention after operation ;the exercise group adopted the treadmill exer-cise(DSPT-1) for 8 weeks .After the exercise ,the Morris maze test was conducted for evaluating the cognitive function in each group .The rats were finally killed for detecting the ChAT activity and AchE activity of hippocampus .Results In the positioning navigation training ,the latency period of the sham operation group was significantly short than that of the exercise group and the model group ,but the latency period of the exercise group was obviously short than that of rats in the model group (P<0 .05);in the spatial exploration test ,the rats in the sham operation group had more frequency of crossing platform than the other two groups ,the exercise group had more frequency of crossing platform in platform quadrant than the model group (P<0 .05);the exercise training could increase the ChAT activity and lower the AchE activity of hippocampus .Conclusion The exercise training can improve the function of hippocampal cholinergic system in SHR/SP and then increase the cognitive ability .

We isolated a novel lectin (AHL) from Artocarpus hypargyreusHance and showed its immunomodulatory activities. In this study, the amino acid sequence of AHL was determined by cDNA sequencing. AHL cDNA (875bp) contains a 456-bp open reading frame (ORF), which encodes a protein with 151 amino acids. AHL is a new member of jacalin-related lectin family (JRLs), which share high sequence similarities to KM+ and Morniga M, and contain the conserved carbohydrate binding domains. The antitumor activity of AHL was also explored using Jurkat T cell lines. AHL exhibits a strong binding affinity to cell membrane, which can be effectively inhibited by methyl-α-D-galactose. AHL inhibits cell proliferation in a time- and dose-dependent manner through apoptosis, evidenced by morphological changes, phosphatidylserine externalization, poly ADP-ribose polymerase (PARP) cleavage, Bad and Bax up-regulation, and caspase-3 activation. We further showed that the activation of ERK and p38 signaling pathways is involved for the pro-apoptotic effect of AHL.