RESUMO
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.
RESUMO
ObjectiveTo examine the protective effects of 17-β estradiol on the experimental model of spinal cord injury (SCI) rats. Methods One hundred and eighty male Sprague Dawley (SD) rats, after Allen' s model, SD rats were divided into three groups: the sham group, the acute spinal cord injury (control groups) and the acute spinal cord injury supplying with 17-β estradiol treatment group. SCI was made by Allen's weight dropping, impacting on the posteriors of spinal cord T10. The content of malonyldialdehyed (MDA), glutathione (GSH), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were determined by chromatometry. The expressions of Caspase-3 and Bcl-2 family in the injured spinal cord were detected by immunohistochemical staining. Results The BBB scores at each time point in 17-β estradiol treatment group were significantly higher than that in SCI group (P<0.05). The contents of GSH, SOD, GSH-Px and the expression of Bcl-2 protein at the majority of time point in 17-β estradiol treatment group were significantly higher than that in SCI group(P<0.05), however, the MDA, Caspase-3 and Bax were markedly decreased (P<0.05). Conclusions This study suggests that 17-β estradiol administration might prevent the cells from SCI-induced apoptosis by triggering to reduce the oxidative stress.