Luteolin attenuates cognitive dysfunction induced by chronic cerebral hypoperfusion through the modulation of the PI3K/Akt pathway in rats
Data publikacji: 05 lip 2021
Zakres stron: 341 - 349
Otrzymano: 19 lis 2020
Przyjęty: 16 cze 2021
DOI: https://doi.org/10.2478/jvetres-2021-0037
Słowa kluczowe
© 2021 H. He, X. Chen. published by Sciendo
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.
Introduction
In our study, we evaluated the beneficial effect of luteolin in the treatment of cognitive dysfunction in rat models induced by cerebral hypoperfusion by two-vessel occlusion (2-VO).
Material and Methods
Seventy-five male Sprague Dawley rats were subjected to 2-VO surgery, in all but 15 (the sham group, group I) the ligation being permanent to impair cognitive abilities. The sham group rats received saline instead of a drug; 15 2-VO rats were not injected at all (the model group, group II); 15 2-VO rats were administered luteolin at 50 mg/kg b.w. (the lut 50 group, group III); to a further 15 luteolin was given at 100 mg/kg b.w. (the lut 100 group, group IV); and the final 15 received nimodipine at 16 mg/kg b.w. as positive controls (the nimodipine group, group V). Object recognition and Morris water maze tests were performed to investigate memory ability. A Western blot test was also conducted to assess expression of phosphatidylinositol 3-kinase (PI3K), its downstream target protein kinase B (Akt), and the phosphorylated form (P-Akt) in cerebral cortex and hippocampus tissue samples.
Results
Significant variations in the discrimination index in the object recognition test, the escape latencies in the Morris water maze test, and expression levels of PI3K-p110α and PI3K-p85 were observed three months after 2-VO surgery in both lut groups, with a significant change in the nimodipine group compared to the model group. P-Akt and Akt were expressed significantly higher in both lut groups and the nimodipine group than in the model group.
Conclusion
Luteolin treatment of rats cognitively dysfunctional after experimental cerebral hypo perfusion was neuroprotective by activating the PI3K/Akt signals which inhibit neuronal death in the cerebral cortex and hippocampal region.