Effect of Borage on hipocampal TNF-α protein and gene in the Amyloid β-Peptide(25–35)-Induced of Alzheimer model in rat

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder and most common form of dementia that leads to memory impairment. In the present study we have examined the investigating effect of Borago officinale on hipocampal TNF-α α α α α protein in the Beta Amyloid peptid induced of inflammation in the rat. Wistar male rats received intrahippocampal (IHP) injection of the Aβ β β β β(25-35) and borage extract orally (100 mg/ kg).inflamation was confirmed by pathologist.in order to measure the expression of the TNF-α α α α α gene , RT-PCR method and for extraction of the TNF-α α α α α protein western bloting method was used. results showed that using Borage lead to reduce TNF-α α α α α gene and protein. This data suggests that borage could improve the reduction of inflammation factors such as TNF-α α α α α and borage consumption may lead to an improvement of ADinduced cognitive dysfunction.

Intranasal Delivery of Human Wharton’s Jelly-Derived Mesenchymal Stem Cells Alleviate Memory Deficits In Sporadic Alzheimer’s Rat Model By Regulating Neurotrophic and Apoptosis Genes

“…These impairments are caused by mainly loss of cholinergic neurons especially in basal forebrain cholinergic neurons (BFCN) as a result of extracellular deposition of Aβ proteins (Senile Plaques) and intracellular formation of neuro brillary tangles (NFTs) in the brain speci cally in the hippocampus region [2,3]. It is reported that these lesions (i. e. Aβ deposition and NFTs formation) can be resulted from decreasing in neurotrophic factors mainly brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) [4] which is nally led to apoptosis and cell death [5]. Hence, apoptosis, also known as programmed cell death, contributes to neuronal cell death in AD as a result of trophic factor deprivation [6].…”

Intranasal Delivery of Human Wharton’s Jelly-Derived Mesenchymal Stem Cells Alleviates Memory Deficits In Sporadic Alzheimer’s Rat Models By Regulating Neurotrophic and Apoptotic Genes

“…These impairments are mainly caused by the loss of cholinergic neurons, especially in basal forebrain cholinergic neurons (BFCN), as a result of extracellular deposition of Aβ proteins (senile plaques) and intracellular formation of neuro brillary tangles (NFTs) in the brain, especially in the hippocampus [2,3]. It has been reported that these lesions (i.e., Aβ deposition and NFT formation) can result from a decrease in neurotrophic factors, mainly the brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) [4], and nally lead to apoptosis and cell death [5]. Therefore, apoptosis, also known as programmed cell death, contributes to neuronal cell death in AD due to trophic factor deprivation [6].…”