Studies On The Palliative Effect Of Deproteinized Calf Blood Extractives Injection On Alzheimer’s Disease

Deproteinized Calf Blood Extractives Injection(DCBEI)is a sterile solution that included inorganics and small molecule organic manufactured from fresh calf blood by deproteinization,ultrafiltration and incrassation.There are more than 200 bioactive constituents contained in DCBEI,and the molecular weight of bioactive constituent less than 5 k Da.DCBEI main points Governance disease brain ischemia,dysneuria and craniocerebral trauma,and also peripheral arterial disease and diabetic polyneuropathy.DCBEI can enhance oxidative metabolism in the brain by improve oxygen utilization and uptake,along with energy metabolism and glucose uptake in mitochondria.Neurodegenerative diseases have been raised concern for a long time,which contains Alzheimer’s disease,Parkinson’s disease,amyotrophic lateral sclerosis,Huntington’s disease and other prototypical examples.With the progress of the study on neurodegenerative diseases,the common characteristics neuronal injury and cell death,meanwhile,mitochondrial involvement,apoptosis and oxidative stress are the important common themes in these diseases.The clinical features of AD are progressive cognitive decline,but its pathogenesis are poorly elucidated due to it is a multifactorial disease.The cognitive decline is characterized by extracellular Aβ plaques and neurofibrillary tangles main caused by P-Tau.Aβ deposited in plaques was deemed has neurotoxic effects in a variety of ways,including Disrupte mitochondrial function by binding alcohol dehydrogenase protein,Inhibite the apoptosis gene through inhibition of insulin signaling,and Aβ also lead to functionally connected groups of neurons will degenerate together.For supplement,after oxidative stress the protein oxidation to lead to Aβ deposition.and Aβ deposition induces the phosphorylation of Tau.Glutamate(Glu)is a neurotransmitter which related to brain excitement,meanwhile high concentration of glutamate associated with ROS excessive accumulation and calcium influx.In AD patients Glu metabolism is impaired,at the same time Glu excessive accumulation,cause a damage of neurons via excitotoxicity.L-glutamate(L-Glu)-induced model of HT22 cellsis an established model related with oxidative stress and Mitochondrial apoptosis process.β-amyloid precursor protein(APP)and Presenilin 1(PS1)are play the important roles in AD,which significantly accelerate the rate of decline in cognitive function lead to AD course acceleration.Currently,B6C3-Tg(APPswe PSEN1 d E9)/Nju(APP/PS1)transgenic mouse model with obvious learning and memory dysfunction at 8?months-old,which has been widespread use in AD pathophysiology study.Based on the foundations,it will be stated that DCBEI protects hippocampal neurons by regulating the mitochondrial apoptosis pathway related to oxidative stress through the L-Glu-induced HT22 cell apoptosis model.In HT22 cells,DCBEI induces the expression of anti-apoptotic proteins(such as Bcl-2 and Bcl-XL)and regulates apoptosis by controlling mitochondrial permeability and inhibiting Cyt-C release.At the same time,the overload of intracellular Ca2 + overload was controlled.APP/PS1 double transgenic mice can express mutant of PS1 and APP fusion bodies,at the same time the mutation of these two genes can increase the content of Aβ,mainly Aβ 1-42.After the treatment of DCBEI,we found that the learning and spatial cognitive impairment and anxiety of APP/PS1 mice were significantly improved.Our results showed that DCBEI could regulate the antioxidant system in a positive way: by protecting the electron transport chain from being destroyed and reducing the production of oxygen free radicals,thus suppressing the oxidative stress in APP/PS1 mice.There are also results show that DCBEI can regulate the expression of neurotransmitters in order to alleviate AD symptoms.And the regulation of neurotransmitters by DCBEI may also be another mechanism to alleviate the pathological symptoms of AD.In this paper,the neuroprotective activity of DCBEI in Alzheimer’s disease(AD)will be systematically studied.To analyze via the combination of proteomics and metabonomics techniques,illustrate the molecular pharmacological mechanism of DCBEI on AD and screen the potential effective targets which were interrelated to AD.In conclusion,the results of our study suggest that DCBEI can alleviate AD symptoms by alleviating apoptosis,regulating oxidative stress,regulating neurotransmitter expression and other biological processes.The results can provide experimental basis for DCBEI to become a drug for treating AD.