Effects of Curcumin and Boric Acid Against Neurodegenerative Damage Induced by Amyloid Beta (1-42)
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Effects of Curcumin and Boric Acid Against Neurodegenerative Damage Induced by Amyloid Beta (1-42) Ceyhan Hacioglu 1
&
Fatih Kar 2 & Ezgi Kar 2 & Yakup Kara 3 & Gungor Kanbak 2
Received: 22 October 2020 / Accepted: 23 November 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Synaptosomes are used as an ex vivo model in the investigation of neuronal transmission and neurodegenerative processes. In this study, we aimed to determine the protective effects of boric acid (BA) and curcumin, which have antioxidant and antiinflammatory properties, on Aβ1-42 induced neurodegenerative damage. Synaptosomes obtained from the rat cerebral cortex were divided into five groups: control, 10 μM Aβ1-42, 10 μM Aβ1-42 + 25 mM BA, 10 μM Aβ1-42 + 10 μM curcumin, and 10 μM Aβ1-42 + 25 mM BA+10 μM curcumin. Synaptosomes treated with Aβ1-42 caused a significant decline in synaptophysin levels and increase in malondialdehyde (MDA) levels, acetylcholinesterase (AChE) activities, DNA fragmentation values, and nitric oxide (NO) levels compared with the control group (P < 0.01). Synaptosomes treated with BA showed a significant reduction in MDA and NO levels against Aβ1-42 exposure (P < 0.01). In addition, curcumin treatment has been found to cause a significant reduction in AChE activities and MDA levels in synaptosomes (P < 0.05). Co-administration of BA and curcumin on synaptosomes exposed to Aβ1-42 resulted in a significant decrease in DNA fragmentation values, MDA levels, and AChE activities. Curcumin and BA + curcumin combination showed an enhancement in synaptophysin levels of Aβ1-42induced synaptosomes (P < 0.01). The results showed that BA and curcumin had protective effects on rat brain synaptosomes against Aβ1-42 exposure. BA and curcumin treatment can have abilities to prevent the alterations of the cholinergic system and inhibit oxidative stress in the cerebral cortex synapses of Aβ1-42 exposed. Keywords Alzheimer’s diseases . Amyloid beta . Boric acid . Curcumin . Neurodegeneration . Oxidative stress . Synaptophysin . Synaptosome
Introduction Alzheimer’s disease (AD) is a neurodegenerative disease related to aging and dementia. Characteristically, AD includes increased production of senile plaques (SPs) and neurofibrillary tangles (NFTs). SPs are formed by irregular aggregates of peptides called amyloid beta (Aβ). NFTs are formed by hyper-phosphorylation of tau protein. Despite increased SPs and NFTs in AD brain, cognitive decline in AD is mostly
* Ceyhan Hacioglu [email protected] 1
Department of Medical Biochemistry, Faculty of Medicine, Duzce University, Duzce, Turkey
2
Department of Medical Biochemistry, Faculty of Medicine, Eskisehir Osmangazi University, Eskisehir, Turkey
3
Department of Chemistry, Faculty of Science, Karadeniz Technical University, Trabzon, Turkey
associated with insoluble Aβ oligomers [1]. Degradation or loss of the synapse structure (rather than SP and NFT accumulations or neuronal loss) is strongly correlated with the cognitive, behavioral, and memo
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