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    Cerebroprotective Effects of Ginsenoside Rg1 on Rats with Amyloid β-Protein Induced Alzheimer’s Disease

    W. Zhou, Z. Chang, Weizhuo Yang and Enhu Jiao
    Indian J Pharm Sci 2022;84(2):493-500

    Abstract The protective mechanism of ginsenoside Rg1 for Alzheimer’s disease induced by Amyloid β-Protein has rarely been reported. To evaluate the cerebroprotective effects of ginsenoside Rg1 on Alzheimer’s disease rats. Male Sprague Dawley rats were randomly divided into 5 groups (n=10). Alzheimer’s disease model was established by injecting Amyloid β-Protein into the hippocampal CA1 area. Rg1 group, specific phosphoinositide 3-kinase inhibitor LY294002 group and Rg1 plus LY294002 group were intraperitoneally injected with corresponding drugs, once daily for 28 consecutive d. The spatial learning and memory abilities were studied by water maze and platform tests respectively. The pathological changes of hippocampal CA1 area were observed by hematoxylin and eosin staining. Neuronal apoptosis was detected by Terminal deoxynucleotidyl transferase dUTP Nick-End Labeling assay. Protein kinase B and Glycogen synthase kinase 3 beta protein expressions were measured by Western blotting. Compared with model group, the learning and memory abilities of Rg1 group were significantly improved (p<0.05), and the abnormal morphology of neurons in Rg1 group and their apoptosis were significantly relieved (p<0.05). Compared with model group, the superoxide dismutase and glutathione peroxidase levels of Rg1 group increased significantly, whereas that of Malondialdehyde decreased significantly (p<0.05). Compared with model group, the Protein kinase B and Glycogen synthase kinase 3 beta phosphorylation levels of Rg1 group significantly increased (p<0.05). LY294002 and Rg1+LY294002 groups had similar results (p>0.05). Ginsenoside Rg1 may mitigate Amyloid β-Protein induced Alzheimer’s disease by activating the phosphoinositide 3-kinase/Protein kinase B/ Glycogen synthase kinase 3 beta signaling pathway, inhibit neuronal apoptosis in the hippocampus and attenuate oxidative stress, exerting cerebroprotective effects.