The neuroprotection of deproteinized calf blood extractives injection against Alzheimer's disease via regulation of Nrf-2 signaling

Abstract

Alzheimer’s disease (AD) is characterized by cognitive decline due to the accumulation of extracellular β-amyloid (Aβ) plaques and neurofibrillary tangles in the brain, which impair glutamate (Glu) metabolism. Deproteinized Calf Blood Extractive Injection (DCBEI) is a biopharmaceutical that contains 17 types of amino acids and 5 types of nucleotides. In this study, we found that DCBEI pretreatment reduced L-Glu-dependent neuroexcitation toxicity by maintaining normal mitochondrial function in HT22 cells. DCBEI treatment also reduced the expression of pro-apoptosis proteins and increased the expression of anti-apoptosis proteins. Furthermore, DCBEI attenuated AD-like behaviors (detected via the Morris water maze test) in B6C3-Tg (APPswePSEN1dE9)/Nju double transgenic (APP/PS1) mice; this effect was associated with a reduction in the amount of Aβ and neurofibrillary tangle deposition and the concomitant reduction of phospho-Tau in the hippocampus. Metabonomic profiling revealed that DCBEI regulated the level of neurotransmitters in the hippocampus of APP/PS1 mice. Label-free proteomics revealed that DCBEI regulated the expression of Nrf-2 and its downstream targets, as well as the levels of phospho-protein kinase B and mitogen-activated protein kinase. Together, these data show that DCBEI can ameliorate AD symptoms by upregulating Nrf2-mediated antioxidative pathways and thus preventing mitochondrial apoptosis.

Salidroside attenuates neuronal ferroptosis by activating the Nrf2/HO1 signaling pathway in Aβ1-42-induced Alzheimer’s disease mice and glutamate-injured HT22 cells

“…The cell viability decreased to 48.15%±1.58% (Fig. 1 D) when cells were exposed to 25 mM of Glu for 24 h. The concentration is consistent with previous studies [ 33 – 35 ] and was chosen in the following experiments. No significant differences were observed in the salidroside groups and the negative control (Fig.…”

Huoxiang Zhengqi alleviates azoxymethane/dextran sulfate sodium-induced colitis-associated cancer by regulating Nrf2/NF-κB/NLRP3 signaling

“…Samples were separated on an ultra-highperformance liquid chromatography system (1,290 Infinity LC, Agilent Technologies, Palo Alto, Calif. United States) equipped with a ACQUITY UPLC BEH Amide 1.7 μm, 2.1 mm × 100 mm column (Waters, Milford, MA, United States) and were analyzed using a quadrupole-time of flight mass spectrometer (AB Sciex TripleTOF 6,600, Framingham, MA, United States). The separation conditions were identical to those reported in previous studies (Qu et al, 2021).…”

Effects of NBP on postoperative cognitive dysfunction in rats via Nrf 2/ARE pathway

“…With the progress of medical technology and the arrival of an aging population in China, the number of elderly patients undergoing surgery will gradually increase. As a result, the number of POCD patients will also increase, and it AGING will cause an enormous economic strain on the country and its families [5]. Therefore, the study of POCD has been the key research direction of anesthesiology, neuroscience, and geriatrics in recent years.…”

“…At present, most of the studies on the Nrf 2/ARE pathway in neurocognitive disorders focus on the downstream products of the Nrf 2/ARE pathway and their effects on oxidative stress and neuronal apoptosis, lacking studies on the direct impact of Nrf 2 on mitochondrial function [ 6 ]. Currently, most of the studies are focused on vascular cognitive impairment (VCI) and Alzheimer's disease (AD), and only a few studies are on POCD [ 5 , 6 ]. Therefore, we conducted this study to investigate the function of the Nrf 2/ARE signaling pathway in POCD through the rat tibial fracture model of POCD and verify the protective effect of the Nrf 2/ARE signaling pathway on POCD through the specific agonists and antagonists of this pathway from the aspects of rat behavior test, hippocampal neuron morphology, hippocampal tissue oxidative stress level, and mitochondrial morphology and dynamics in hippocampal neuronal cells.…”