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Cerebroprotective effects of ginsenoside rg1 on rats with amyloid beta-protein induced alzheimer’s disease

By: Wang, Lishui.
Contributor(s): Shen, Song.
Publisher: Mumbai Indian Journal of Pharmaceutical Science 2022Edition: Vol.84(2), Mar-Apr.Description: 493-500p.Subject(s): PHARMACEUTICSOnline resources: Click here In: Indian journal of pharmaceutical sciencesSummary: The protective mechanism of ginsenoside Rg1 for Alzheimer’s disease induced by amyloid beta-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 beta-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 beta-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.
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The protective mechanism of ginsenoside Rg1 for Alzheimer’s disease induced by amyloid beta-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 beta-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 beta-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.

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