Olfactory Ensheathing Cell-Conditioned Medium Reverts Aβ25–35-Induced Oxidative Damage in SH-SY5Y Cells by Modulating the Mitochondria-Mediated Apoptotic Pathway

Abstract

9 Abstract Olfactory ensheathing cells (OECs) are a type of 10 glia from the mammalian olfactory system, with neuro-11 protective and regenerative properties. b-Amyloid peptides 12 are a major component of the senile plaques characteristic 13 of the Alzheimer brain. The amyloid beta (Ab) precursor 14 protein is cleaved to amyloid peptides, and Ab 25-35 is 15 regarded to be the functional domain of Ab, responsible for 16 its neurotoxic properties. It has been reported that Ab [25][26][27][28][29][30][31][32][33][34][35] 17 triggers reactive oxygen species (ROS)-mediated oxidative 18 damage, altering the structure and function of mitochon-19 dria, leading to the activation of the mitochondrial intrinsic 20 apoptotic pathway. Our goal is to investigate the effects of 21 OECs on the toxicity of aggregated Ab [25][26][27][28][29][30][31][32][33][34][35]

The conditioned medium of human mesenchymal stromal cells reduces irradiation-induced damage in cardiac fibroblast cells

“…UC-MSCs cells were maintained in DMEM containing 10% FBS in uncoated 25 cm 2 culture flasks (Corning, New York, USA) at 37°C in 5% CO2. When the cell culture reached about 70–80% confluence, the MSCCM was replaced with medium containing 1% FBS and cultured for 2–3 days, then collected, filtered through a membrane of 0.2 mm pore, aliquoted and stored at –20°C [ 13 ]. The same method was used to generate the conditioned medium from MRC-5 cells as a control, called MRCCM.…”

Protective Effects of Wogonin against Alzheimer’s Disease by Inhibition of Amyloidogenic Pathway

“…Mitochondria are targets of A β that accumulates in the membrane of mitochondria, and mitochondrial function is disrupted in an early phase of AD [ 11 – 15 ], suggesting that A β aggregation is involved in mitochondria-mediated apoptosis [ 16 , 17 ]. It has been reported that A β leads to cytochrome C release through mitochondrial membrane permeabilization [ 18 , 19 ] that induces mitochondrial-mediated apoptosis.…”

Study on Calceolarioside A Anti‐Aβ25–35‐Induced Damage in SH‐SY5Y cells by Atomic Force Microscopy

“…The SH‐SY5Y cells were used to research the protection of nerve cells for Alzheimer's disease [16] and screening medicine or functional foods in vitro [17,18] . It was reported that the IC 50 of Aβ 25–35 on SH‐SY5Y cells was 40 mM [3] . In this article, the toxicity of low concentration of Aβ 25–35 in SH‐SY5Y cells and whether Calceolarioside A can reverse the damage were studied.…”

“…The clinical feature of AD is cognitive decline, which involves the parts of the brain that control thought, learning, memory and language. [3] There are many scientists currently studying AD and related problems, however, people still cannot explain the pathogenesis and causes of Alzheimer's disease. It is known that the peptide of Aβ accumulation will damage the cells in brain, even leads to the cell death, and is related to the development of AD, and eventually, leads to the obstacles in human cognitive functions.…”