Ginkgo biloba extract 50 dropping pills improve vascular cognitive impairment through anti-oxidative and...

The aim of the present study was to investigate the improvement effect of Ginkgo biloba extract 50 dropping pill (GBE50DP) on vascular cognitive impairment (VCI) induced by cerebral ischemia and its mechanism. The VCI rat model was established by 2-vessel occlusion and randomly divided into the control, model, positive and GBE50DP administration groups. The administration groups were then administered GBE50DP intragastrically for 8 weeks. The social behavior and ability of learning and memory of each group were tested through the Morris water maze and eight-arm maze experiment. The content of oxidative stress and inflammatory factors in the hippocampus of rats were detected using ELISA. Hematoxylin & eosin staining and Terminal-deoxynucleotidyl transferase mediated nick end labeling staining were used to observe the morphological changes of nerve cells in the hippocampal CA1 region of rats. The expression of Caspase-3, Bcl-2, Bax, cytochrome c (Cyto-C), fibroblast-associated antigen (Fas) and poly(ADP-ribose) polymerase-1 (PARP-1) proteins in the hippocampal CA1 region of rats was detected by immunohistochemistry and western blot analysis. The blood components of GBE50DP were analyzed using liquid chromatography-tandem mass spectrometry. The model rats showed significant cognitive impairment; compared with the model group, in the GBE50DP administration groups, the social behavior of rats was markedly improved; the content of superoxide dismutase, glutathione peroxidase and catalase in the hippocampus was markedly increased and that of malondialdehyde, IL-1β, IL-6 and TNF-α was significantly decreased. The pathological changes and expression of Cyto-C, Bax, Bcl-2, Caspase-3, Fas and PARP-1 proteins in brain tissue were markedly improved. The index components of GBE50DP in blood included ginkgolide A, B, C and K and bilobalide, as well as flavonoids such as rutin and quercetin. In conclusion, GBE50DP improved the social behavior, ability of learning and memory in VCI rats, decreased nerve cell damage and protected nerve cells from apoptosis by reducing oxidative stress and inflammation, thereby improving cognitive dysfunction.