ABSTRACT
ObjectiveIn order to investigate anti-ageing mechanisms of the notoginsenoside Rg1,we used Aβ_(1-42) and D-galactose to establish aging rat model. Methods Ninety rats were divided into three groups at random: sham group, model group, treatment group. Aging rat models were established by injecting peritoneally D-galactose (100 mg/kg) to the rats for 56 days and after 35 days aggregated Aβ_(1-42)(μg) was injected to the right lateral ventricle of rats. Meantime, rats were treated by intragastric administration the notoginsenoside Rg1. Then spatial memory of experimental rats was examined with the Morris water maze(MWM). The thiol antioxidants including glutathione reductase (GR) and glutathione peroxidase (GSH-Px) activities were examined by colorimetric method. The concentration of the pro-caspase-3 and Bcl-2 were examined by the immunohistochemistry and Western blotting method. Results In aging model rats escape latercies were significantly prolonged (P<0.05), while decreases were seen in the time of staying the third quadrants of platform, the number of crossing over a platform, the concentration of the GR, GSH-Px, and pro-caspase-3 as compared with the sham group(P<0.05). After treatment of the notoginsenoside Rg1, the aging model rats exhibited significant increases in the time of staying the third quadrants of platform, the number of crossing over a platform, the concentration of the GR, GSH-Px, and pro-caspase-3(P<0.05), while a decrease was observed in escape latercies as compared to control group(P<0.05). Moreover there was no significant difference in the expression of the Bcl-2(P>0.05). Conclusion The results from our study indicate that the notoginsenoside Rg1 could improve the oriented learning and memory capacity and prevent the neurodegeneration of central nervous systems in aging model rats by up-regulating the expression of the thiol antioxidants(including GR and GSH-Px) and resisting the cleavage of the pro-caspase-3.
ABSTRACT
Objective To explore the effects of notoginsenoside-Rg_1 on brain-derived neurotrophic factor(BDNF) protein in cerebrum cortex of MCAO/R injury,as well as to investigate whether notoginsenoside-Rg_1 can up-regulate the protein content of BDNF of the positive neurons or the amount of the po-sitive neurons.Methods Adult male SD rats(60) were randomly divided into model group,notoginsenoside-Rg_1 high,middle,and low dose(200,100,50 mg/kg) groups,and the positive control(Nimodipine,1 mg/kg) group.All drugs were given once a day by ip till the mouse was killed.The focal cerebral(ischemia-)reperfusion model was made with thread-occluded method.Their frozen brain tissue were sliced(into) section of 12 ?m thickness.The four rats were randomly taken from each groups to be treated as specimens after surgical handle in 1,3,and 7 d.The slices were according to the immunohistochemical ABC techniques.The protein content of BDNF of the positive neurons and the amount of the positive neurons in cerebrum cortex of rat were observed and counted by HPIAS—1000 analytic system,and the nervous deficit symptoms after the cerebral ischemia were observed.Results Comparing with the model group,all notoginsenoside-Rg_1 treated groups obviously improved some nervous deficit symptoms of cerebral ischemia-reperfusion rats,and increased the protein content of BDNF and the amount of the positive neurons in the cerebrum cortex of model rats(P
ABSTRACT
Objective:To study the effect of notoginsenoside-Rg 1 on immunoinflammatory injury in rat model of Parkinson′s disease.Methods:The rat model of Parkinson′s disease was established and treated with notoginsenoside-Rg 1 by injecting in the striatum.The change of rotational behavior,levels cytokines in striatum and splenocyte proliferation were measured.Results:After treatment with notoginsenoside-Rg 1 the rotational behavior and levels of TNF-?,IL-1?,IL-6 were decreased.The splenocyte proliferation was increased.Conclusion:Notoginsenoside-Rg 1 can regulate the immunological function and reduce the pathological injury to dopaminergic neuron caused by immunoinflammatory reaction.