Coenzyme Q10 Protects Human Endothelial Cells from β-Amyloid Uptake and Oxidative Stress-Induced Injury

Abstract

Neuropathological symptoms of Alzheimer's disease appear in advances stages, once neuronal damage arises. Nevertheless, recent studies demonstrate that in early asymptomatic stages, ß-amyloid peptide damages the cerebral microvasculature through mechanisms that involve an increase in reactive oxygen species and calcium, which induces necrosis and apoptosis of endothelial cells, leading to cerebrovascular dysfunction. The goal of our work is to study the potential preventive effect of the lipophilic antioxidant coenzyme Q (CoQ) against ß-amyloid-induced damage on human endothelial cells. We analyzed the protective effect of CoQ against Aβ-induced injury in human umbilical vein endothelial cells (HUVECs) using fluorescence and confocal microscopy, biochemical techniques and RMN-based metabolomics. Our results show that CoQ pretreatment of HUVECs delayed Aβ incorporation into the plasma membrane and mitochondria. Moreover, CoQ reduced the influx of extracellular Ca2+, and Ca2+ release from mitochondria due to opening the mitochondrial transition pore after β-amyloid administration, in addition to decreasing O2 .− and H2O2 levels. Pretreatment with CoQ also prevented ß-amyloid-induced HUVECs necrosis and apoptosis, restored their ability to proliferate, migrate and form tube-like structures in vitro, which is mirrored by a restoration of the cell metabolic profile to control levels. CoQ protected endothelial cells from Aβ-induced injury at physiological concentrations in human plasma after oral CoQ supplementation and thus could be a promising molecule to protect endothelial cells against amyloid angiopathy.

Comparative Study on the Influence of Epigallocatechin-3-gallat e and/ or Coenzyme Q10 against Alzheimer's disease Induced by Aluminium in Normally-Fed and Protein Malnourished Rats

“…Moreover, the present results may be also explained based on the potential role of CoQ10 in the treatment of neurodegenerative damages associated AD [89]. It is also reported that pre-treatment with CoQ10 prevents Aβ accumulation; it can reduce the influx of extracellular Ca 2+ , and Ca 2+ release from mitochondria due to opening the mitochondrial transition pore after β-amyloid uptake [90]. CoQ10 treatment can also decrease plaque area and number in the hippocampus as well as in the cortex [91] which is in agreement with the results of the histopathological examinations obtained in the current study.…”

Differential effects of graphene materials on the metabolism and function of human skin cells

“…The NMR experiments were carried out using a Varian Inova 500 spectrometer operating at 499.77 MHz for 1 H and at 125.678 MHz for 13 C. The spectrometer was equipped with a four-nucleus 5 mm 1 H { 15 N-31 P}PFG high-field indirect detection probe. Standard 1D spectra with water suppression ( presat) were recorded as previously reported by us 80 with a spectral width of 8 kHz, 32k data points, a 90°pulse width of 11.5 µs, a 4 s relaxation delay and 400 scans, at 298 K and using pulse sequences from the Varian library. Manual phase and baseline corrections were applied to all 1D spectra for processing.…”

“…Apoptotic nuclei were determined according to morphological criteria. 80 For viability, necrosis and apoptosis, the results are expressed as percentage vs. total cells (n = 4).…”

Regulation of the oxidative balance with coenzyme Q10 sensitizes human glioblastoma cells to radiation and temozolomide

“…Cells were grown onto 25 cm2 flasks and treated for 24 h with vehicle (ethanol; control) or 5 lM CoQ. The level of lactate, glutamate, glycine, serine and glutamine was assessed as described before [24].…”