Effects of diesel exhaust particles and urban particles on brain endothelial cells.
Ji Young KimSeonmi HongOchirpurev BolormaaJe Hoon SeoSang-Yong EomYong Dae KimHeon KimPublished in: Toxicological research (2021)
Exposure to diesel exhaust particles (DEPs) and urban particles (UPs) increases the incidence of degenerative brain diseases as well as respiratory diseases. However, there is limited evidence on the mechanism of neurotoxicity on exposure to these particles. In the present study, the damage to blood-brain barrier (BBB) function by DEP or UP exposure was evaluated in bEnd.3 cells, which are derived from the brain tissue of Balb/c mice. It was demonstrated that DEP and UP exposure may induce oxidative stress via increasing reactive oxygen species (ROS) and decreasing total antioxidant capacity (TAC) level in bEnd.3 cells. In addition, cells exposed to DEP and UP demonstrated a resistance value of about 50% each compared to the value noted prior to exposure; additionally, Claudin-5 and ZO-1 expression levels were significantly decreased compared to the corresponding levels in the control. It was inferred that DEP or UP exposure diminishes the expression of tight junction proteins in endothelial cells through ROS generation, thereby enhancing endothelial membrane permeability. This study showed that DEPs or UPs induced cell permeability and oxidative stress by increasing ROS generation in bEnd.3 cells. This suggests the possibility that exposure to DEPs or UPs may compromise the integrity of the BBB and induce adverse effects in the CNS.
Keyphrases
- blood brain barrier
- induced apoptosis
- oxidative stress
- endothelial cells
- reactive oxygen species
- cell cycle arrest
- dna damage
- cell death
- endoplasmic reticulum stress
- poor prognosis
- cerebral ischemia
- high glucose
- diabetic rats
- particulate matter
- type diabetes
- adipose tissue
- metabolic syndrome
- single cell
- skeletal muscle
- binding protein
- multiple sclerosis
- air pollution
- mesenchymal stem cells
- subarachnoid hemorrhage