Abstract
BackgroundExposure to airborne fine particulate matter (PM2.5) has been reported to be harmful to the human kidney. However, whether the activation of oxidative stress and cell apoptosis plays key roles in the nephrotoxicity caused by PM2.5 exposure is still poorly understood. The aim of this study was to explore the mechanism of cytotoxicity after PM2.5 exposure in human proximal tubule epithelial cells (HK-2 cells).ResultsPM2.5 exposure resulted in a significant decrease in cell viability, with an increase in LDH release and the early kidney damage marker kidney injury molecule-1 (KIM-1) expression in a dose-dependent manner and time-dependent manner. PM2.5 exposure induced reactive oxygen species (ROS) generation and markedly elevated apoptosis in HK-2 cells. In addition, PM2.5 exposure resulted in the activation of antioxidant pathway, as evidenced by the increased expressions of Nrf2, HO-1 and NQO1 and decreased expression of Keap1. Moreover, PM2.5 exposure also induced the activation of apoptotic pathway, as evidenced by the increased expressions of pro-apoptotic proteins Bax, caspase-3 and caspase-8 and decreased expression of antiapoptotic protein Bcl-2.ConclusionsOur results demonstrated that both antioxidant pathway and apoptotic pathway played critical roles in the damage mediated by PM2.5 in HK-2 cells. This study would give us a strategy to prevent the impairment of renal function by PM2.5 induced through repression of oxidative stress and apoptosis.
Highlights
Exposure to airborne fine particulate matter (PM2.5) has been reported to be harmful to the human kidney
Our results demonstrated that both antioxidant pathway and apoptotic pathway played critical roles in the damage mediated by PM2.5 in human proximal tubule epithelial cells (HK-2) cells
This study would give us a strategy to prevent the impairment of renal function by PM2.5 induced through repression of oxidative stress and apoptosis
Summary
Exposure to airborne fine particulate matter (PM2.5) has been reported to be harmful to the human kidney. The aim of this study was to explore the mechanism of cytotoxicity after PM2.5 exposure in human proximal tubule epithelial cells (HK-2 cells). The potential adverse effects of ambient fine particulate matter (PM2.5, aerodynamic diameter ≤ 2.5 μm) on public health have caused significant concerns worldwide. Huang et al Environ Sci Eur (2020) 32:2 some epidemiological studies have reported a strong and consistent association between P M2.5 exposure and reduced kidney function as well as an increased rate of renal function decline [5,6,7]. The mechanism of P M2.5-induced renal dysfunction remains unclear
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