Flavonoid glycoside fraction of <i>Ginkgo biloba</i> extract modulates antioxidants imbalance in vanadium-induced brain damage

Adeshina O. Adekeye; Adedamola A. Fafure; Morayo M. Omodele; Lawrence D. Adedayo; Victor O. Ekundina; Damilare A. Adekomi; Ephraim Samuel Jen; Thomas K. Adenowo; Adeshina O. Adekeye; Adedamola A. Fafure; Morayo M. Omodele; Lawrence D. Adedayo; Victor O. Ekundina; Damilare A. Adekomi; Ephraim Samuel Jen; Thomas K. Adenowo

doi:10.3934/Neuroscience.2023015

AIMS Neuroscience

2023, Volume 10, Issue 2: 178-189. doi: 10.3934/Neuroscience.2023015

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Research article Topical Sections

Flavonoid glycoside fraction of Ginkgo biloba extract modulates antioxidants imbalance in vanadium-induced brain damage

1.
Department of Anatomy, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Ekiti State, Nigeria
2.
Department of Physiology, College of Health Sciences, Bowen University, Iwo, Osun State, Nigeria
3.
Department of Medical Laboratory Science, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Ekiti State, Nigeria
4.
Department of Anatomy, Faculty of Basic Medical Sciences, College of Health Sciences, Osun State University, Osogbo, Nigeria
5.
Department of Anatomy, Faculty of Basic and applied Sciences, Lead City University, Ibadan, Oyo State, Nigeria

Received: 13 January 2023 Revised: 14 June 2023 Accepted: 26 June 2023 Published: 29 June 2023

Human and animal diseases have always been reported to be treated by medicinal herbs owing to their constituents. Excess sodium metavanadate is a potential environmental toxin when consumed and could induce oxidative damage leading to various neurological disorders and Parkinsons-like diseases. This study is designed to investigate the impact of the flavonoid Glycoside Fraction of Ginkgo Biloba Extract (GBE) (at 30 mg/kg body weight) on vanadium-treated rats. Animals were divided randomly into four groups: Control (Ctrl, normal saline), Ginkgo Biloba (GIBI, 30mg/kg BWT), Vanadium (VANA, 10 mg/kg BWT) and Vanadium + Ginkgo biloba (VANA + GIBI). Markers of oxidative stress (Glutathione Peroxidase and Catalase) were assessed and found to be statistically increased with GIBI when compared with CTRL and treatment groups. Results from routine staining revealed that the control and GIBI group had a normal distribution of cells and a pronounced increase in cell count respectively compared to the VANA group. When compared to the VANA group, the NeuN photomicrographs revealed that the levels of GIBI were within the normal range (***p < 0.001; ** p < 001). The treatment with GIBI showed a better response by increasing the neuronal cells in the VANA+GIBI when compared with the VANA group. The NLRP3 Inflammasome photomicrographs denoted that there was a decrease in NLRP3-positive cells in the control and GIBI groups. The treatment group shows fewer cells compared to that of the VANA group. The treatment group shows fewer cells compared to that of the VANA group. The findings of the study confirmed that ginkgo biloba extract via its flavonoid glycoside fraction has favorable impacts in modulating vanadium-induced brain damage with the potential ability to lower antioxidant levels and reduce neuroinflammation.
- ginkgo biloba extract,
- inflammasome,
- vanadium,
- NeuN,
- Glutathione peroxidase
Citation: Adeshina O. Adekeye, Adedamola A. Fafure, Morayo M. Omodele, Lawrence D. Adedayo, Victor O. Ekundina, Damilare A. Adekomi, Ephraim Samuel Jen, Thomas K. Adenowo. Flavonoid glycoside fraction of Ginkgo biloba extract modulates antioxidants imbalance in vanadium-induced brain damage[J]. AIMS Neuroscience, 2023, 10(2): 178-189. doi: 10.3934/Neuroscience.2023015

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Abstract

Human and animal diseases have always been reported to be treated by medicinal herbs owing to their constituents. Excess sodium metavanadate is a potential environmental toxin when consumed and could induce oxidative damage leading to various neurological disorders and Parkinsons-like diseases. This study is designed to investigate the impact of the flavonoid Glycoside Fraction of Ginkgo Biloba Extract (GBE) (at 30 mg/kg body weight) on vanadium-treated rats. Animals were divided randomly into four groups: Control (Ctrl, normal saline), Ginkgo Biloba (GIBI, 30mg/kg BWT), Vanadium (VANA, 10 mg/kg BWT) and Vanadium + Ginkgo biloba (VANA + GIBI). Markers of oxidative stress (Glutathione Peroxidase and Catalase) were assessed and found to be statistically increased with GIBI when compared with CTRL and treatment groups. Results from routine staining revealed that the control and GIBI group had a normal distribution of cells and a pronounced increase in cell count respectively compared to the VANA group. When compared to the VANA group, the NeuN photomicrographs revealed that the levels of GIBI were within the normal range (***p < 0.001; ** p < 001). The treatment with GIBI showed a better response by increasing the neuronal cells in the VANA+GIBI when compared with the VANA group. The NLRP3 Inflammasome photomicrographs denoted that there was a decrease in NLRP3-positive cells in the control and GIBI groups. The treatment group shows fewer cells compared to that of the VANA group. The treatment group shows fewer cells compared to that of the VANA group. The findings of the study confirmed that ginkgo biloba extract via its flavonoid glycoside fraction has favorable impacts in modulating vanadium-induced brain damage with the potential ability to lower antioxidant levels and reduce neuroinflammation.

Acknowledgments

We sincerely appreciate the management of Afe Babalola University for graciously providing the enabling environment with adequate cutting edge facilities to carry out this research and for giving permission to collaborate with other universities.

Conflict of interest

The authors declare no conflict of interest.

Author contributions

AOA conceived the conceptual idea, AOA, AAF, and MMO conducted the experiments and planned the literature search. AAF and VOE analyzed and interpreted the data. AOA, AAF DDA, LDA and TKA drafted the manuscript, read, revised the manuscript. All authors gave the final approval for the manuscript to be published.

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